Albey BSc N

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Hepatitis A (HAV) | Pathophysiology | Signs and symptoms | Treatment | Nursing Management

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Hepatitis A (HAV) is a highly contagious liver infection caused by the hepatitis A virus. It is commonly transmitted through the ingestion of contaminated food or water or through close contact with an infected person. The virus primarily affects the liver, leading to symptoms such as fatigue, nausea, vomiting, abdominal pain, jaundice (yellowing of the skin and eyes), and dark urine.

Most cases of hepatitis A resolve on their own within a few weeks to months, and there is typically no long-term liver damage. However, in some cases, particularly in older adults or those with underlying liver disease, hepatitis A can lead to severe complications and even liver failure, although this is rare. Preventive measures for hepatitis A include vaccination, practicing good hygiene such as thorough handwashing, and avoiding consuming contaminated food or water. Vaccination is highly effective in preventing hepatitis A and is recommended for individuals at increased risk of infection, including travelers to regions with high rates of hepatitis A, people with chronic liver disease, men who have sex with men, and illicit drug users.

Fecal-oral transmission

Hepatitis A is primarily transmitted through the fecal-oral route, where the virus is shed in the feces of an infected individual and then ingested orally by another person. This transmission can occur through contaminated food or water, inadequate sanitation practices, or poor personal hygiene. Individuals can become infected by consuming food or water contaminated with the virus or by coming into contact with surfaces or objects contaminated with infected feces and then touching their mouth.

Spread by direct contact

The virus can also spread through direct contact with an infected person. This can happen through activities such as caring for an infected individual, changing the diapers of an infected child, or engaging in sexual activity with an infected partner. Close personal contact with someone who has hepatitis A increases the risk of transmission.

  • Ingestion of contaminated food, milk, or water: Contaminated food, milk, or water serves as a vehicle for hepatitis A transmission. Food handlers who are infected and fail to practice proper hand hygiene after using the restroom can contaminate food during preparation, leading to the spread of the virus to others who consume the contaminated food. Similarly, drinking water from contaminated sources can also result in infection.
  • Parenteral transmission: Although rare, hepatitis A can be spread parenterally, meaning through exposure to infected blood or blood products. This mode of transmission is less common compared to fecal-oral transmission but can occur through practices such as sharing needles or other equipment used for injecting drugs.
  • Prevalence: Hepatitis A is more prevalent in underdeveloped countries and areas with overcrowded and poorly sanitized conditions. These environments facilitate the spread of the virus through contaminated food, water, and inadequate hygiene practices.
  • Incubation period: The incubation period for hepatitis A typically ranges from 2 to 6 weeks. During this time, an infected individual may not show any symptoms but can still transmit the virus to others. This period between exposure to the virus and the onset of symptoms is crucial for understanding and managing the spread of the disease.

Pathophysiology of hepatitis

A, the hepatitis A virus (HAV) initially invades hepatocytes, the liver cells, upon entering the body through ingestion or contact. Once inside the liver cells, the virus begins to replicate, leading to their destruction. As the virus proliferates, it triggers an immune response from the body, resulting in the production of antibodies targeted at combating HAV.

The immune response is crucial in the body’s defense against hepatitis A. Antibodies generated in response to the virus aid in neutralizing and clearing the virus from the bloodstream, thereby limiting its spread and preventing further damage to liver cells. This immune response also contributes to the inflammatory process observed in hepatitis A infection.

As the immune system works to eliminate the virus, hepatocytes undergo a process of destruction, regeneration, and repair. Liver cells damaged by the virus are gradually replaced through the regeneration of healthy hepatocytes. This process allows the liver to resume its normal functions over time.

Individuals who recover from hepatitis A typically develop immunity against future infections. This immunity is conferred by the presence of antibodies specific to HAV, which provide long-term protection against reinfection. Thus, once an individual has experienced hepatitis A and recovered, they are generally considered immune for the rest of their life.

Overall, the pathophysiology of hepatitis A involves a complex interplay between viral invasion, immune response, liver cell damage, and regeneration, ultimately leading to recovery and the development of long-lasting immunity in most cases.

Signs and symptoms of hepatitis

A can vary in severity, with some individuals experiencing mild or no symptoms at all. However, even in cases where symptoms are absent or mild, the individual remains contagious, as the virus can still be present in their feces and transmitted to others.

Common symptoms of hepatitis A infection include:

  • A brief, mild illness resembling flu-like symptoms.
  • Nausea, vomiting, and diarrhea.
  • Loss of appetite leads to weight loss.
  • Fever, indicating the body’s immune response to the virus.
  • Jaundice, characterized by yellowing of the skin and the whites of the eyes, is due to liver dysfunction.
  • Darker yellow urine.
  • Pale or clay-colored stools, reflecting disruptions in bile production and flow.
  • Itchy skin is a result of accumulated bilirubin in the bloodstream.
  • Abdominal pain, particularly in the right upper quadrant (hypochondriac region),.

In some cases, diarrhea may also occur as a symptom of a hepatitis A infection. The infection typically resolves within two months, although in some individuals, symptoms may persist longer or recur intermittently. It’s essential to seek medical attention if symptoms persist or worsen, as hepatitis A can occasionally lead to complications such as liver failure.

Overall, recognizing the signs and symptoms of hepatitis A is crucial for prompt diagnosis and management to prevent further transmission and complications associated with the infection.

Diagnosing hepatitis A involves several steps

  • Patient history: Begin by obtaining a comprehensive patient history to assess potential risk factors for hepatitis A infection, such as recent travel to endemic regions or exposure to contaminated food or water.
  • Clinical evaluation: Conduct a thorough clinical examination to evaluate symptoms and signs suggestive of hepatitis A, such as jaundice, abdominal pain, and liver enlargement.
  • Laboratory testing: Confirm the diagnosis of hepatitis A through appropriate laboratory testing, which typically involves detecting specific antibodies to the hepatitis A virus (HAV). This is done using serological tests, particularly the detection of IgM antibodies against HAV. Additionally, consider performing serologic testing to rule out hepatitis A infection in individuals presenting with unexplained acute liver failure.
  • Exclusion of other liver diseases: In cases of unexplained acute hepatitis, it’s essential to exclude other potential causes, such as hepatitis B or C infection. This can be achieved through blood tests to detect markers of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection.
  • Liver function tests: Perform a comprehensive assessment of liver function through laboratory evaluation, including tests for urine bilirubin and urobilinogen, as well as serum levels of total and direct bilirubin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, prothrombin time, total protein, albumin, and immunoglobulins (IgG, IgA, and IgM).
  • Imaging studies: Consider conducting liver imaging studies, such as liver scans, to evaluate for any structural changes or abnormalities in the liver.
  • Stool and urine analysis: Collect stool samples for electron microscopy to detect the presence of viral particles, and assess urine for urobilinogen levels, which can indicate liver dysfunction.

Treatment for hepatitis

A typically involves supportive care and the management of symptoms. Specific interventions may include:

  • Fluid therapy: Administer intravenous fluids to prevent dehydration, such as a 5% dextrose solution, especially if nausea and vomiting are present.
  • Anti-emetics: Prescribe anti-emetic medications, such as promethazine (Phenergan), to alleviate nausea and vomiting.
  • Antihistamines: Use antihistamines like promethazine to control itching, a common symptom of hepatitis A.
  • Rest: Advise the patient to get plenty of rest to promote recovery and alleviate fatigue.
  • Glucose: Provide glucose to support the metabolic needs of the liver and aid in its recovery.
  • Vitamins: Administer vitamin supplements, including vitamin B complex and vitamin A, to support liver function and overall health.
  • Steroids: In some cases, corticosteroids like prednisolone may be prescribed to reduce inflammation and alleviate symptoms. The dosage and duration should be determined by a healthcare professional.
  • Analgesics: Recommend pain relievers such as paracetamol (acetaminophen) to manage abdominal pain. Ensure adherence to the recommended dosage and duration to avoid liver damage.

It’s important to note that there is no specific antiviral treatment for hepatitis A, as the infection typically resolves on its own without causing chronic liver disease. However, supportive measures can help alleviate symptoms and promote recovery.

Patients should also be advised to avoid alcohol and certain medications that may exacerbate liver damage during the acute phase of the illness. Close monitoring of liver function and symptoms is essential, and patients should follow up with healthcare providers as needed for ongoing care and management.

Prevention of hepatitis A infection

To prevent hepatitis A infection, it’s crucial to implement various measures within the community:

  • Clean water supply: Ensure access to clean and safe drinking water by maintaining and improving water treatment and distribution systems. Regular testing of water quality is essential to identify and address potential contamination.
  • Good sanitation: Promote proper sanitation practices, including the safe disposal of human waste and sewage. Implementing effective sewage treatment systems and proper waste management techniques can help prevent the spread of hepatitis A through contaminated water sources.
  • Good personal hygiene: Educate community members about the importance of good personal hygiene, including frequent handwashing with soap and water, especially after using the restroom and before handling food. Proper hand hygiene can significantly reduce the risk of transmitting hepatitis A and other infectious diseases.
  • Vaccination against hepatitis A: Encourage community members to receive the hepatitis A vaccine, which provides long-term protection against the virus. Vaccination is particularly important for individuals at high risk of infection, such as travelers to endemic regions, healthcare workers, and those with chronic liver disease.
  • Prophylaxis with anti-hepatitis A immunoglobulin: In situations where immediate protection against hepatitis A is needed, such as during outbreaks or following exposure to the virus, prophylaxis with anti-hepatitis A immunoglobulin may be recommended. This provides temporary passive immunity against the virus and can help prevent infection or reduce its severity.
  • Avoiding overcrowding: Implement measures to reduce overcrowding in living spaces, schools, healthcare facilities, and other community settings. Overcrowding can facilitate the transmission of infectious diseases like hepatitis A, so promoting social distancing and adequate spacing between individuals is essential for disease prevention.

Nursing Management

When assessing a patient for hepatitis A infection, healthcare providers can conduct a comprehensive history and physical examination to aid in diagnosis and management. Here’s what can be included:

  1. History

    • Travel history: Inquire about recent travel to regions with high hepatitis A prevalence, as exposure to contaminated food or water in these areas increases the risk of infection.
    • Exposure history: Determine if the patient has been in contact with individuals known to have hepatitis A or has been exposed to contaminated food, water, or other potential sources of infection.
    • Symptom onset: Ask about the onset and duration of symptoms such as nausea, vomiting, abdominal pain, jaundice, and fatigue, as well as any associated factors or exacerbating factors.
    • Medical history: Obtain information about the patient’s medical history, including any underlying liver disease, previous hepatitis A infection or vaccination, and any medications or supplements currently being taken.
    • Social history: Assess for risk factors such as substance abuse, sexual practices, and living or working conditions that may increase the likelihood of hepatitis A transmission.

  2. Physical Examination

    • Jaundice: Assess for yellowing of the skin and sclera (whites of the eyes), which is a common sign of hepatitis A due to liver dysfunction.
    • Abdominal tenderness: palpate the abdomen for tenderness or pain, particularly in the right upper quadrant, which may indicate liver inflammation.
    • Liver enlargement: Perform palpation of the liver to assess for hepatomegaly, which can occur in hepatitis A as a result of liver inflammation and swelling.
    • Skin manifestations: Look for signs of itching or rash, which may be present in some individuals with hepatitis A.
    • General appearance: Evaluate the patient’s overall appearance and demeanor for signs of fatigue, malaise, or other symptoms suggestive of hepatitis A infection.

Nursing Care

Aims

  1. Patient Isolation:
    • Interventions:
      1. Implement standard precautions to prevent transmission of hepatitis A to other patients and healthcare workers.
      2. Consider placing the patient in single-room isolation to minimize the risk of spreading the virus to others.
      3. Educate the patient and visitors about the importance of hand hygiene and the proper disposal of contaminated materials.
      4. Use personal protective equipment, such as gloves and gowns, when providing direct care to the patient.
  2. Infection Prevention:
    • Interventions:
      1. Ensure strict adherence to hand hygiene protocols among healthcare staff, patients, and visitors.
      2. Regularly clean and disinfect high-touch surfaces and equipment in the patient’s environment.
      3. Encourage respiratory hygiene practices, such as covering coughs and sneezes with a tissue or elbow, to prevent the spread of respiratory droplets.
      4. Provide education on proper food handling and sanitation practices to prevent foodborne transmission of hepatitis A.
  3. Disease Notification:
    • Interventions:
      1. Notify public health authorities of confirmed cases of hepatitis A according to local reporting requirements.
      2. Collaborate with public health officials to identify and notify individuals who may have been exposed to the virus.
      3. Provide information and resources to the community about hepatitis A prevention and vaccination.
      4. Maintain the confidentiality and privacy of patient information in accordance with healthcare regulations.
  4. Environment:
    • Interventions:
      1. Ensure a clean and safe environment for the patient by regularly cleaning and disinfecting surfaces and equipment.
      2. Minimize environmental triggers that may exacerbate symptoms, such as strong odors or loud noises.
      3. Provide comfortable and supportive furnishings to promote rest and relaxation.
      4. Implement measures to reduce the risk of falls or injuries, especially if the patient experiences weakness or fatigue.
  5. Observation:
    • Interventions:
      1. Monitor the patient’s vital signs regularly to assess for signs of worsening illness or complications.
      2. Observe for changes in mental status, behavior, or level of consciousness that may indicate hepatic encephalopathy.
      3. Monitor for signs of dehydration, such as decreased urine output or dry mucous membranes, and intervene promptly.
      4. Document and report any significant changes in the patient’s condition to the healthcare team for further evaluation and management.
  6. Psychological Care:
    • Interventions:
      1. Provide emotional support and reassurance to the patient and their family members, addressing concerns and fears about the illness.
      2. Encourage open communication and provide opportunities for the patient to express their feelings and emotions.
      3. Offer relaxation techniques and stress-reduction strategies to help alleviate anxiety and promote emotional well-being.
      4. Collaborate with other members of the healthcare team, such as social workers or counselors, to provide additional support as needed.
  7. Hygiene:
    • Interventions:
      1. Assist the patient with personal hygiene activities, such as bathing, grooming, and oral care, as needed.
      2. Provide education on proper handwashing technique and encourage frequent hand hygiene.
      3. Ensure access to clean and comfortable clothing and bedding, changing linens regularly to maintain hygiene.
      4. Monitor for signs of skin breakdown or irritation and implement measures to prevent pressure ulcers or infections.
  8. Exercises:
    • Interventions:
      1. Encourage the patient to engage in gentle physical activities, such as walking or stretching, as tolerated.
      2. Provide guidance on appropriate exercises to promote circulation, muscle strength, and flexibility.
      3. Monitor the patient during exercise sessions and adjust activities as needed based on their energy level and symptoms.
      4. Collaborate with physical therapists or rehabilitation specialists to develop a personalized exercise plan for the patient’s recovery.
  9. Nutrition:
    • Interventions:
      1. Assess the patient’s nutritional status and dietary preferences to develop a suitable meal plan.
      2. Offer small, frequent meals and snacks to maintain adequate energy intake and prevent malnutrition.
      3. Emphasize the importance of a balanced diet rich in nutrients, including protein, carbohydrates, vitamins, and minerals.
      4. Provide education on foods to avoid, such as alcohol and fatty or spicy foods, which may exacerbate liver inflammation.
  10. Elimination:
    • Interventions:
      1. Monitor the patient’s bowel habits and assess for any changes in stool consistency or frequency.
      2. Encourage adequate fluid intake to prevent dehydration and promote regular bowel movements.
      3. Provide education on the importance of maintaining good bowel habits and preventing constipation.
      4. Administer laxatives or stool softeners as prescribed to alleviate constipation and promote bowel regularity.
  11. Medication:
    • Interventions:
      1. Administer medications as prescribed by the healthcare provider, ensuring accurate dosage and timing.
      2. Monitor for potential side effects or adverse reactions to medications, and intervene as needed.
      3. Educate the patient about the purpose, dosage, and potential side effects of prescribed medications.
      4. Ensure proper storage and handling of medications to maintain their efficacy and safety.
  12. Advice at Discharge:
    • Interventions:
      1. Provide written and verbal instructions on self-care measures, including hygiene practices, dietary modifications, and medication management.
      2. Schedule follow-up appointments with healthcare providers for ongoing monitoring and evaluation of the patient’s recovery.
      3. Offer resources and referrals for additional support services, such as community health programs or support groups.
      4. Emphasize the importance of the hepatitis A vaccination for household contacts and close contacts to prevent further transmission of the virus.

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Typhoid Fever | Causes | Sign and Symptoms | Pathophysiology | Nursing Management

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Typhoid fever, also known as enteric fever, is a systemic infectious disease caused by Salmonella typhi. It is characterized by lesions in the Peyer’s patches, mesentery, and spleen. Typical symptoms include a high fever that fluctuates, along with malaise, headaches, and abdominal pain.

Causative Organism

Salmonella typhi is a bacterium belonging to the Salmonella genus, specifically known for causing typhoid fever in humans. This bacterium has a rod-shaped structure and is gram-negative. It primarily infects the gastrointestinal tract, leading to symptoms characteristic of typhoid fever, such as fever, abdominal pain, and gastrointestinal disturbances. Salmonella typhi is susceptible to various methods of disinfection, including drying, pasteurization, and common disinfectants used in sanitation.

Reservoir of Infection

Humans are the primary reservoir of infection for typhoid fever. Individuals with active cases of the disease, as well as carriers who harbor the bacterium in their bodies, can transmit the infection to others. Carriers may be individuals who have recovered from typhoid fever but continue to shed the bacteria in their stool or urine, either temporarily during the convalescent period or as chronic carriers. This makes the identification and management of carriers critical to preventing the spread of the disease. Without appropriate treatment, carriers can unknowingly transmit the infection to others, contributing to outbreaks of typhoid fever.

Source of Infection

The primary sources of typhoid fever infection are the feces and urine of individuals with active cases or carriers. The bacterium is shed in high numbers through the feces and urine of infected individuals, especially during the acute phase of the illness. Contamination of water sources and food items with fecal or urine matter containing Salmonella typhi bacteria is a significant mode of transmission. Additionally, poor sanitation practices, such as improper disposal of sewage or a lack of handwashing, can contribute to the spread of the infection. Secondary sources of infection include contaminated water, food, hands, and flies that come into contact with infected feces or urine. Proper sanitation, hygiene practices, and access to clean water are crucial in preventing the transmission of typhoid fever. Public health measures, such as vaccination campaigns and health education programs, also play a vital role in controlling the spread of the disease.

Environmental and Social Factors

The incidence of typhoid fever tends to increase during the rainy season, coinciding with a rise in the fly population. Outside of the human body, Salmonella typhi bacteria, the causative agent of typhoid fever, can be found in various environmental sources such as water, ice, food, milk, and soil. The survival duration of the bacteria varies depending on the environmental conditions. While typhoid bacilli do not multiply in water, many of them can perish within 48 hours to 7 days.

However, they may survive for extended periods, such as over a month in ice and ice cream, up to 70 days in soil irrigated with sewage under moist conditions, and about 30 days or more in dry conditions. Notably, the bacilli can multiply and persist in food, particularly milk. Vegetables grown in sewage farms or washed in contaminated water pose a significant health hazard. Social factors also contribute to the spread of the disease, including contaminated water supplies, open-air defecation and urination, and low standards of food and personal hygiene.

Incubation Period

The typical incubation period for typhoid fever ranges from 10 to 14 days. However, depending on the dose of the bacilli ingested, it may manifest in as little as 3 days or extend up to 21 days.

Mode of TransmissionTyphoid fever is primarily transmitted through the oral-fecal route, usually via ingestion of contaminated water and food, especially raw fruits and vegetables. This mode of transmission underscores the importance of ensuring access to clean water and promoting proper food handling and hygiene practices to prevent the spread of the disease.

Pathophysiology

Infection occurs through the ingestion of the organism, which swiftly penetrates the intestinal mucosa and proliferates within the intestinal lumen for a brief period. During the first four days of the incubation period, stools may test positive for the organism upon culturing. Subsequently, the organisms migrate to the mesenteric lymph nodes from the mucosa. Following a short period of multiplication in these nodes, the organisms enter the bloodstream via the thoracic duct, causing transient primary bacteremia. They are then transported to the liver and spleen. After further multiplication at these sites, a vast number of organisms enter the bloodstream, leading to the onset of clinical illness characterized by secondary bacteremia.

Throughout this secondary bacteremia phase, which predominates during the illness, nearly all organs are susceptible to invasion. However, the involvement of the gall bladder and Peyer’s patches in the lower small intestine holds clinical significance. The gall bladder is likely infected via the liver, resulting in subclinical cholecystitis. The presence of infected bile renders stool cultures positive. Chronic bile infection may develop in individuals with pre-existing gall bladder disease, leading to chronic fecal carriage.

Invasion of the Peyer’s patches can occur either during the primary intestinal infection or during the secondary bacteremia phase, with further dissemination facilitated through infected bile. The Peyer’s patches undergo hyperplasia, accompanied by infiltration of chronic inflammatory cells. Subsequent necrosis of the superficial layer results in the formation of irregular, ovoid ulcers along the long axis of the gut, mitigating the likelihood of stricture formation post-healing. In cases where an ulcer erodes into a blood vessel, severe hemorrhage ensues, while transmural perforation leads to peritonitis.

Clinical Manifestations of Typhoid Fever

The course of untreated typhoid fever unfolds across four distinct stages, each lasting approximately one week. Symptoms can vary in intensity, ranging from mild to severe.

Week 1: During the initial week, symptoms are nonspecific, with an insidious onset in adults but potentially abrupt in children. Early manifestations include:

  • Severe headache
  • Malaise
  • Loss of appetite (anorexia)
  • Generalized body aches
  • Epistaxis (nosebleeds)
  • Remittent fever characterized by a gradual rise in temperature to about 40°C by the week’s end
  • Mild, non-productive cough (bronchitis)
  • Constipation
  • Enlargement and tenderness of the spleen, leading to abdominal pain

Week 2: In the second week, patients often appear prostrate and toxic, accompanied by a sustained high temperature of around 40°C. Additional symptoms may include:

  • Confusion and disorientation, with possible hallucinations
  • Slight abdominal distension and tenderness in the right lower quadrant
  • Delirium and agitation earned the condition the nickname “nervous fever.”
  • Development of rose spots, which are 2mm to 4mm-diameter pink papules that fade upon pressure. They typically emerge between the 7th and 12th days on the upper abdomen and lower chest. Rose spots result from bacterial embolization, and cultures of these spots may yield positive results.
  • Relative bradycardia is characterized by a pulse rate lower than expected for a patient with a fever.

Week 3: During the third week of typhoid fever, the patient’s condition typically worsens as they become more toxic and ill. The following manifestations may occur:

  • A continuous high fever persists.
  • Delirium continues, with the patient experiencing confusion and disorientation.
  • Abdominal distension becomes more pronounced, accompanied by scanty bowel sounds.
  • Crackles may develop over the lung bases.
  • Diarrhea becomes prominent, with the patient experiencing 6 to 8 stools per day. The stool may be green and foul-smelling, resembling pea soup.
  • Hepatosplenomegaly (enlargement of the liver and spleen) and elevation of liver transaminases are observed.
  • Considerable weight loss occurs due to the prolonged illness.
  • The Widal reaction, a serological test for typhoid fever, shows strongly positive results with anti-O and anti-H antibodies.
  • Blood cultures may still be positive at this stage.

Several complications may arise during the third week:

  • Intestinal hemorrhage may occur due to bleeding in congested Peyer’s patches. While serious, it is usually not fatal.
  • Intestinal perforation in the distal ileum is a severe complication that can be frequently fatal. It may manifest without alarming symptoms until septicemia or diffuse peritonitis develops.
  • Encephalitis and neuropsychiatric symptoms, such as “muttering delirium” or “coma vigil,” may occur, with the patient exhibiting behaviors like picking at beddings or imaginary objects.
  • Metastatic abscesses, cholecystitis, endocarditis, and osteitis may develop.
  • Dehydration becomes more pronounced, and the patient remains delirious, entering a state known as the typhoid state.
  • By the end of the third week, the fever begins to subside.

Week 4: In patients who survive, the following changes occur during the fourth week:

  • The fever, mental state, and abdominal distention gradually improve over a few days, although intestinal complications may still arise.
  • Convalescence is typically a slow process, requiring time for the patient to fully recover from the effects of the illness.

Prognosis

The prognosis for typhoid fever is generally favorable with early diagnosis and appropriate treatment.

Nursing Management 

Investigations

  • Full Blood Count: This test may reveal mild leukocytosis, leukopenia, neutropenia, normocytic anemia, and mild thrombocytopenia.
  • Elevated serum transaminases and mild proteinuria may be observed.
  • Blood and bone marrow cultures: These cultures can isolate the causative organism, providing a definitive diagnosis.
  • Faecal and urine cultures: Faecal cultures typically yield positive results during the first week, serving as presumptive evidence of the infection. Urine cultures may be positive less frequently.
  • Serology: The Widal test is commonly used and will be positive. However, it’s important to note that the Widal reaction detects antibodies to the causative organism, but it has limitations. Patients with previous immunizations against typhoid fever or those who have had other Salmonella infections may also test positive.
  • The detection of IgG and IgM antibodies may also aid in diagnosis.

Drug Therapy Treatment of Cases

Antibiotics

  • Ciprofloxacin: Oral administration of 750mg twice daily for 14 days. If persistent vomiting occurs, 400mg intravenous infusion every 12 hours for 7 days can be administered.
  • Amoxicillin: Oral dosage of 500mg every 8 hours for 2 weeks.
  • Co-trimoxazole: Oral intake of 960mg twice daily for 1 week.
  • Azithromycin: A single oral dose of 500mg followed by 250mg daily from day 2 to day 7.

Antipyretic drug:

  • Paracetamol: Oral dosage of 1g three times daily for 5 days.

Fluid and Electrolyte Replacement Therapy:

  • Treatment should be tailored to the level of dehydration present in the patient.

Prevention and Control of Typhoid Fever

There are generally three lines of defense against typhoid fever:

  1. Control of Reservoirs and Cases:
  • Early Diagnosis: Recognizing the early symptoms, which are often nonspecific, is crucial. Blood and stool cultures are important diagnostic tools.
  • Notification: Cases should be promptly reported following established notification procedures.
  • Isolation: Given the infectious nature and prolonged course of typhoid fever, patients should be isolated in healthcare facilities until three consecutive bacteriologically negative stools and urine reports are obtained.
  • Treatment: Administer appropriate and effective treatment to patients.
  • Disinfection: Stool and urine are the primary sources of infection and should be handled in closed containers and disinfected using recommended methods. Soiled clothing and linens should also be disinfected. Strict handwashing practices should be observed by all individuals in contact with the patient and contaminated items.
  • Follow-up: Regular follow-up examinations of stools and urine should be conducted for Salmonella typhi 3 to 4 months after the patient’s discharge and again after 12 months to prevent the development of the carrier state.

Carriers

  • Identification: Carriers are identified through cultural and serological examinations. The presence of Salmonella in the biliary tract of carriers can be confirmed through duodenal drainage.
  • Treatment: Carriers should undergo an intensive course of effective drug therapy to eliminate the bacteria.
  • Surveillance: Carriers should be closely monitored to prevent transmission to others. They should refrain from handling food, milk, or water for others.
  • Information, Education, and Communication (IEC): Education initiatives should emphasize the importance of handwashing with soap after defecation or urination and before preparing food. Other key messages include the use of toilets or pit latrines, control of fly populations, and terminal disinfection of all contaminated articles.

Control of Sanitation

  • Protection and Purification of Water Supplies: Measures such as water treatment and ensuring the safety of water sources are essential to prevent contamination with Salmonella typhi.
  • Improvement of Basic Sanitation: Enhancing sanitation infrastructure, including the construction of toilets and proper waste disposal facilities, is crucial in preventing fecal-oral transmission of bacteria.
  • Promotion of Food Hygiene: Educating individuals on proper food handling and storage practices helps prevent contamination of food with Salmonella typhi, reducing the risk of infection.

Mass Immunization with Typhoid Vaccine

  • Individuals residing in endemic areas: Mass immunization programs target individuals living in areas where typhoid fever is prevalent. This population is at higher risk of exposure to the Salmonella typhi bacterium due to contaminated water sources, poor sanitation, and overcrowded living conditions. Vaccinating residents helps build immunity within the community, reducing the overall incidence of typhoid fever and preventing outbreaks.
  • Household contacts of typhoid fever patients: Close contacts of typhoid fever patients, such as family members and caregivers, are at increased risk of contracting the disease due to direct exposure to the infected individual. Immunizing household contacts provides a protective barrier against transmission within the home environment, preventing secondary cases and limiting the spread of the infection to other members of the community.
  • Groups at risk of infection, including school children and hospital staff: Certain groups face an elevated risk of typhoid fever due to their living or working conditions. School children may be exposed to contaminated food or water sources in educational settings, while hospital staff may come into contact with infected patients during the course of their duties. Immunizing these at-risk groups helps protect vulnerable populations and minimizes the risk of typhoid outbreaks in high-transmission settings such as schools and healthcare facilities.
  • Travelers planning to visit endemic areas: Individuals traveling to regions where typhoid fever is endemic are at increased risk of infection. Factors such as unfamiliar food and water sources, limited access to clean drinking water, and poor sanitation practices in certain destinations heighten the likelihood of exposure to the Salmonella typhi bacterium. Vaccination before travel provides travelers with a crucial layer of protection against typhoid fever, reducing the risk of illness and ensuring a safer travel experience.

Paratyphoid Fever

  • Paratyphoid fever, caused by Salmonella paratyphi types A, B, or C, shares similarities with typhoid fever but is generally less severe. The pathological and clinical features closely resemble those of typhoid fever, though paratyphoid fever may manifest primarily as acute gastroenteritis in some cases.
  • Pathogenesis: Like typhoid fever, paratyphoid fever is primarily transmitted through the ingestion of contaminated food or water containing the Salmonella paratyphi bacterium. Upon entry into the body, the bacterium targets the intestinal mucosa, leading to gastrointestinal symptoms and potential systemic spread.
  • Clinical Presentation: Patients with paratyphoid fever typically present with symptoms such as fever, headache, malaise, abdominal pain, and gastrointestinal disturbances including nausea, vomiting, diarrhea, or constipation. These symptoms may vary in severity depending on the individual’s immune response and the specific strain of Salmonella paratyphi involved.
  • Distinguishing Features: While paratyphoid fever shares many similarities with typhoid fever, there are some distinguishing features. Paratyphoid fever tends to be milder in comparison, with a lower likelihood of developing severe complications such as intestinal hemorrhage or perforation. Additionally, paratyphoid fever may present with a more pronounced focus on gastrointestinal symptoms, resembling acute gastroenteritis rather than the systemic illness seen in typhoid fever.
  • Diagnosis: Diagnosis of paratyphoid fever involves clinical evaluation, including a thorough medical history and physical examination, as well as laboratory testing. Blood cultures, stool cultures, and serological tests may be utilized to confirm the presence of Salmonella paratyphi and differentiate paratyphoid fever from other similar illnesses.
  • Treatment: Treatment of paratyphoid fever typically involves antimicrobial therapy similar to that used for typhoid fever. Antibiotics such as fluoroquinolones, azithromycin, or third-generation cephalosporins may be prescribed based on the antimicrobial susceptibility profile of the infecting strain. Supportive care to manage symptoms and prevent dehydration may also be indicated.
  • Prevention: Preventive measures for paratyphoid fever focus on ensuring food and water safety, practicing good hygiene, and vaccination in high-risk populations. Improving sanitation, promoting safe food handling practices, and enhancing access to clean drinking water are essential for preventing the transmission of Salmonella paratyphi and reducing the burden of paratyphoid fever. Vaccination against paratyphoid fever may be recommended for individuals at increased risk of exposure, such as travelers to endemic regions or those living in areas with high rates of disease transmission.

Overall, while paratyphoid fever shares similarities with typhoid fever, its milder nature and distinct clinical features underscore the importance of accurate diagnosis and appropriate management to ensure optimal patient outcomes.

Nursing Care for Typhoid and Paratyphoid Fever

Close monitoring of vital signs

Record temperature, pulse, blood pressure, and respirations every 4 hours, or more frequently if abnormalities are noted. Report any abnormalities to the nurse in charge or doctor promptly. Avoid administering aspirin due to the risk of gastric irritation. Monitor for signs of intestinal bleeding such as melena (dark, tarry stools) and hypotension (low blood pressure).

Isolation to Prevent Cross-Infection

Practice meticulous hand hygiene after each contact with the patient, using soap and water or an alcohol-based hand rub. Wear gloves when handling feces, vomit, or soiled bed linens, and dispose of them carefully. Ensure proper disposal of all excretions and rubbish from the patient’s room. Thoroughly disinfect bedpans and vomit bowls after each use. Clean and disinfect all articles used by the patient, including surfaces and medical equipment. Dispose of soiled linen properly according to hospital protocols. Provide handwashing facilities for the patient to promote good hygiene practices.

Careful Monitoring of Fluid Balance

Document all fluid intake and output on a fluid balance chart to monitor hydration status accurately. Intravenous infusion may be necessary to maintain adequate hydration, especially if oral intake is limited due to gastrointestinal symptoms. Encourage oral fluid intake if the patient is able to tolerate it, to prevent dehydration and support recovery.

Nutritional Support

Provide small, frequent meals that are easily digestible and rich in nutrients to support the patient’s energy needs and promote recovery. Monitor dietary intake and assess for any signs of malnutrition or inadequate nutrition. Consider dietary modifications or supplements as needed to meet the patient’s nutritional requirements.

Symptom Management

Administer prescribed medications promptly, including antibiotics and antipyretics, to manage fever and bacterial infections. Monitor for and manage symptoms such as abdominal pain, nausea, and vomiting to improve patient comfort and well-being. Provide appropriate pain relief and comfort measures as needed.

Patient Education

Educate the patient and family members about the nature of the illness, its mode of transmission, and preventive measures to reduce the risk of spread. Emphasize the importance of strict adherence to infection control practices, including hand hygiene and environmental sanitation. Provide guidance on dietary modifications and fluid intake to support recovery and prevent dehydration.

Relieving Abdominal Pain

Administer prescribed analgesics, such as pethidine or morphine, to alleviate severe abdominal pain. Monitor the effectiveness of the analgesia by regularly assessing the patient’s pain levels and communicating with medical staff if pain relief is inadequate. Assist the patient with comfortable positioning to alleviate discomfort and promote relaxation.

Maintaining Hygiene

Assist the patient with a bed bath to maintain cleanliness and promote good skin integrity. Ensure thorough cleaning of the anal region if the patient is experiencing diarrhea to prevent skin breakdown and irritation. Provide regular mouth care to reduce the risk of oral infections and alleviate dry mouth. Implement pressure area care measures to prevent pressure ulcers and skin breakdown. Change bed linen as needed, ensure proper disposal of soiled linen, and maintain a clean and hygienic environment. Provide handwashing facilities for the patient to encourage proper hygiene practices.

Assisting with elimination

Position the patient near the toilet or keep a bedpan readily available to facilitate easy access for elimination. Record stool type on the chart and promptly inform medical staff of any abnormalities or concerns. Ensure privacy and dignity for the patient during toileting activities. Place the patient on a plastic sheet and draw sheet if experiencing diarrhea to maintain cleanliness and ease cleaning. Provide handwashing facilities to promote proper hand hygiene after toileting.

Providing nutrition and fluids

Offer a high-calorie, low-fiber diet to meet the patient’s nutritional needs while minimizing gastrointestinal discomfort. Consider a soft or liquid diet, which may be more easily tolerated and managed by the patient, especially during periods of illness or abdominal pain. Monitor the patient’s dietary intake and fluid consumption, making adjustments as needed to ensure adequate hydration and nutrition.

Complications of Typhoid Fever:

  1. Intestinal Hemorrhage
    • This complication arises when the sloughs covering the Peyer’s patches in the intestines separate, typically during the late second or early third week of the illness.
    • Signs and Symptoms:
      • Sudden drop in body temperature and blood pressure, accompanied by a rapid heartbeat.
      • Passage of bright red blood per rectum, although it may not always be present, especially in cases of paralytic ileus.
    • Management: Patients often require sedation to manage pain and anxiety, along with blood transfusions to address significant blood loss.
  2. Intestinal Perforation
    • Similar to intestinal hemorrhage, this complication occurs when the sloughs covering the Peyer’s patches separate, usually during the late second or early third week of the illness.
    • Signs and Symptoms:
      • Recognizing perforation can be challenging, but symptoms may include worsening pain and tenderness, increased pulse rate, sudden drop in body temperature, presence of free fluid in the abdomen, and demonstration of gas under the diaphragm.
    • Immediate surgical intervention is often necessary to repair the perforation and prevent further complications such as peritonitis.
  3. Complications in the Liver, Gallbladder, and Pancreas
    • Typhoid fever can lead to various complications in these organs, including hepatitis (inflammation of the liver), cholangitis (infection of the bile ducts), cholecystitis (inflammation of the gallbladder), and pancreatitis (inflammation of the pancreas). These complications can result in severe abdominal pain, jaundice, and digestive disturbances.
  4. Cardiorespiratory Complications
    • Typhoid fever can cause toxic myocarditis, which involves inflammation of the heart muscle and can lead to symptoms such as tachycardia, weak pulse, hypotension, and abnormalities on electrocardiogram (ECG). Additionally, patients may develop bronchitis, bronchopneumonia, or lobar consolidation, leading to respiratory symptoms such as cough, difficulty breathing, and chest pain.
  5. Complications in the Nervous System
    • Typhoid fever can affect the nervous system, leading to a range of neurological complications including toxic confusional state (manifesting as disorientation, delirium, and restlessness), facial twitching or convulsions, paranoid psychosis or catatonia, meningitis (inflammation of the meninges), and encephalomyelitis (inflammation of the brain and spinal cord). These complications can result in altered mental status, seizures, and other neurological deficits.
  6. Hematological and Renal Complications
    • Typhoid fever can lead to various hematological complications such as subclinical disseminated intravascular coagulation (DIC), hemolysis (destruction of red blood cells), immune complex glomerulitis (inflammation of the kidney’s filtration units), and nephrotic syndrome (a kidney disorder characterized by proteinuria, edema, and hypoalbuminemia). These complications can result in abnormalities in blood clotting, anemia, and kidney dysfunction.
  7. Musculoskeletal Complications
    • Typhoid fever can also affect the musculoskeletal system, leading to complications such as arthritis (inflammation of the joints) and osteomyelitis (infection of the bones). These complications can result in joint pain, swelling, and restricted movement, as well as bone pain and tenderness.

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Cholera | Causes | Pathogenesis | Signs and Symptoms | Nursing Management

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Cholera is a bacterial infection caused by the bacterium Vibrio cholerae. It typically spreads through contaminated water and food, particularly in areas with poor sanitation and hygiene practices. Cholera can lead to severe diarrhea and dehydration, and in severe cases, it can be life-threatening if not promptly treated. Symptoms of cholera include profuse, watery diarrhea, vomiting, and muscle cramps. Treatment usually involves rehydration therapy, including oral rehydration solution (ORS) or intravenous fluids, along with antibiotics to shorten the duration of illness and reduce the severity of symptoms. Prevention strategies include improving sanitation, ensuring access to clean drinking water, and promoting good hygiene practices such as handwashing. Vaccines are also available to provide protection against cholera in high-risk populations.

Incubation Period: Cholera has an incubation period ranging from a few hours to up to 5 days. During this time, individuals may be infected with the Vibrio cholerae bacterium but not yet display symptoms.

Transmission: The primary mode of transmission for cholera is the oral-fecal route, typically occurring through the ingestion of contaminated food and water. Poor sanitation and hygiene practices contribute to the spread of the disease, particularly in areas with inadequate access to clean water and sanitation facilities.

Causative Organism

Cholera is caused by the bacterium Vibrio cholerae. There are two main biotypes:

  1. Classical cholerae vibrio: This biotype of Vibrio cholerae is responsible for the majority of cholera cases worldwide.
  2. Haemolytic El Tor vibrio: This biotype is a variant of Vibrio cholerae that emerged in the 20th century and is associated with some cholera outbreaks.

Characteristics of Vibrio Cholerae:

  1. Shape: Vibrio cholerae is characterized by its comma shape, resembling a curved rod.
  2. Oxygen Requirement: It is an aerobic organism, meaning it requires oxygen to survive and grow.
  3. Gram Stain: Vibrio cholerae is Gram-negative, indicating that it does not retain the crystal violet stain in the Gram staining process.
  4. Spore Formation: It does not form spores, distinguishing it from certain other bacteria that can produce spores for survival.
  5. Motility: Vibrio cholerae is a motile organism, possessing both flagella and somatic antigens that enable it to move actively.
  6. Heat and Disinfectant Sensitivity: It is susceptible to heat, being killed at temperatures of 55°C for 15 minutes. Additionally, it can be effectively eliminated by phenolic and hypochlorite disinfectants.
  7. Environmental Survival: Vibrio cholerae can survive in aquatic environments for extended periods, entering a dormant state that allows it to persist until conditions become favorable for growth and reproduction.

Epidemiology:

Cholera predominantly affects individuals from low socioeconomic backgrounds residing in areas with poor sanitation, limited access to healthcare services, and unsafe water supplies. The disease is particularly prevalent in regions of Asia and Africa where these conditions are widespread. Cholera transmission occurs primarily through the ingestion of contaminated feces and water. Additionally, consumption of other perishable foods such as milk, cold-cooked dishes, and unwashed fruits and vegetables can also contribute to the spread of infection.

Pathogenesis:

Vibrio cholerae primarily resides in the gut and does not enter the bloodstream. It attaches to the mucosa of the small intestines using outer membrane proteins and flagella adhesions. The bacterium produces an enterotoxin that leads to excessive loss of fluid and electrolytes. This enterotoxin inhibits the absorption of sodium chloride, leading to its excretion along with water, potassium, and bicarbonate. Natural infection typically results in immunity to both the cholera toxin and bacterial surface antigens.

Signs and symptoms:

Evacuation Phase:

  1. Onset of diarrhea ranging from mild to acute, initially containing fecal matter but later becoming watery, often described as “rice water stool.”
  2. Projectile vomiting may accompany diarrhea.
  3. Severe dehydration occurs due to extensive fluid loss from diarrhea and vomiting.

Collapse Phase:

  1. Muscle cramps develop due to electrolyte imbalances resulting from fluid loss.
  2. Metabolic acidosis manifests with signs of air hunger, characterized by deep and sometimes rapid breathing.
  3. Hypovolemic shock ensues due to vascular depletion, leading to vascular collapse. Symptoms include hypotension, tachycardia, and impalpable pulses at the wrist, along with cold, clammy skin, and oliguria. Without intervention, shock can progress to acute renal failure and, potentially, death.

Recovery Phase:

As the patient enters the recovery phase, there is a noticeable improvement in their condition, and the signs and symptoms begin to subside.

  1. Resolution of Symptoms: The diarrhea and vomiting gradually diminish, and the patient experiences a reduction in the severity and frequency of bowel movements and episodes of vomiting.
  2. Hydration Restoration: With appropriate rehydration therapy and fluid replacement, the patient’s hydration status improves. Intravenous fluids or oral rehydration solutions help replenish lost fluids and electrolytes, aiding in the restoration of normal hydration levels.
  3. Regaining Strength: The patient starts to regain strength and energy as they recover from the debilitating effects of dehydration and metabolic disturbances. Muscle weakness and fatigue begin to diminish, allowing the patient to resume normal activities gradually.
  4. Normalization of Vital Signs: Vital signs, such as blood pressure, heart rate, and respiratory rate, stabilize and return to normal ranges as the patient’s condition improves.
  5. Resumption of Appetite: As the gastrointestinal symptoms subside, the patient’s appetite typically returns. They may start to tolerate oral intake better and resume eating a normal diet.

Diagnosis:

Clinical Diagnosis in Epidemics: In epidemic situations, a presumptive diagnosis of cholera is often based on clinical presentation or epidemiological factors. For instance, individuals aged 5 years or older who develop acute watery diarrhea with or without vomiting, particularly in areas where cholera outbreaks are likely to occur, may be clinically diagnosed with the disease.

Laboratory Diagnosis:

  1. Dark Field Microscopy: Examination of stool samples under dark field microscopy may reveal the characteristic darting movement of Vibrio cholerae. Inhibition of this movement by specific antisera (e.g., O1 antisera) provides strong supportive evidence for the diagnosis.
  2. Microbiological Culture: Stool, vomitus, or rectal swabs are collected for microbiological culture and sensitivity testing. This method confirms the presence of Vibrio cholerae in the samples, aiding in a definitive diagnosis.
  3. Immunofluorescent Assay: Immunofluorescent techniques allow for rapid diagnosis of cholera by detecting specific antigens associated with Vibrio cholerae in clinical specimens. This method offers a quick and efficient means of confirming the presence of the bacteria.

Management

Aims:

  1. Correcting Fluid and Electrolyte Imbalance: The primary aim is to restore normal fluid and electrolyte levels in the body to mitigate the effects of dehydration and electrolyte disturbances.
  2. Eliminating the Causative Organism: Efforts are focused on eradicating the Vibrio cholerae bacterium from the body to halt the progression of the disease and prevent further transmission.
  3. Preventing the Spread of Infection: Implementation of measures to contain and control the spread of cholera, including isolation of affected individuals, proper sanitation practices, and hygiene protocols to minimize the risk of transmission to others.
  4. Preventing Complications from Fluid and Electrolyte Loss: Proactive measures are taken to prevent and manage complications arising from severe dehydration and electrolyte imbalances, such as hypovolemic shock, metabolic acidosis, and organ failure. This involves prompt rehydration therapy and close monitoring of the patient’s clinical status.

Therapy:

Correction of Fluid and Electrolyte Imbalance: Immediate initiation of intravenous fluid therapy is essential for correcting fluid and electrolyte imbalances. Use fluids such as Ringer’s lactate or normal saline. If the patient is able to drink, administer oral rehydration solution (ORS) while setting up the intravenous drip.

In cases of severe dehydration, administer rapid intravenous fluid resuscitation, giving 30 mL/kg body weight within the first 30 minutes, followed by 70 mL/kg body weight over the next 2½ hours. The goal is to restore normal hydration and acid-base balance within 2-3 hours. Subsequently, continue rehydrating the patient at a slower rate until the pulse and blood pressure return to normal.

Once the patient is capable of oral intake, provide oral rehydration at a rate of 5 mL/kg body weight per hour (250 mL/hr). Monitor vital signs every 30 minutes during fluid resuscitation, adjusting the rate of infusion if signs of circulatory overload are observed.

Monitor urine output hourly, aiming for a normal range of 30–40 ml/hr. If urine output is reduced, indicating potential acute renal failure, prompt medical intervention is necessary.

Administer ORS as soon as the patient is able to drink orally. Maintain fluid replacement by accounting for losses from stool. Oral rehydration should be encouraged and administered as needed.

Antimicrobial Agents:

  1. Tetracycline: Administer 500mg orally four times a day for a duration of three days. Tetracycline is effective in treating cholera and helps eradicate Vibrio cholerae from the body.
  2. Doxycycline: A single dose of 300mg is considered the drug of choice for cholera treatment. Doxycycline exhibits potent antibacterial activity against Vibrio cholerae and aids in resolving the infection.
  3. Cotrimoxazole: Prescribe 960mg orally twice daily for a duration of three days. Cotrimoxazole, a combination of sulfamethoxazole and trimethoprim, is another option for treating cholera effectively.
  4. Ciprofloxacin: Administer 500mg orally twice daily for three days. Ciprofloxacin is a broad-spectrum antibiotic with activity against Vibrio cholerae, making it suitable for cholera treatment.
  5. Erythromycin: Prescribe 500mg orally four times a day for three days. Erythromycin is effective in treating cholera and can be used as an alternative antimicrobial agent in cases where other antibiotics are not suitable.

These antimicrobial agents help eliminate the causative organism, Vibrio cholerae, from the body, contributing to the resolution of cholera infection and preventing its complications. It is crucial to adhere to the prescribed dosage and duration of treatment to ensure effectiveness and minimize the risk of antimicrobial resistance.

Nursing Management

Patient Isolation:

  1. Implement strict isolation protocols to prevent the spread of infections to other patients and healthcare workers.
  2. Ensure the patient is placed in a designated isolation room with appropriate signage to alert staff and visitors.
  3. Provide personal protective equipment (PPE) to all healthcare workers entering the isolation area.
  4. Limit visitors and ensure they adhere to infection control measures, such as hand hygiene and wearing PPE.
  5. Educate the patient and family members on the importance of isolation and adherence to infection control practices.

Infection Prevention:

  1. Emphasize the importance of hand hygiene to the patient, family members, and healthcare staff, promoting regular handwashing with soap and water or alcohol-based hand sanitizer.
  2. Ensure proper disposal of contaminated materials and disinfection of patient care areas.
  3. Educate the patient and family members on respiratory hygiene, including covering coughs and sneezes with a tissue or elbow.
  4. Implement environmental cleaning protocols to maintain a clean and sanitized patient care environment.
  5. Monitor and enforce adherence to infection prevention practices among healthcare staff through regular audits and education sessions.

Disease Notification:

  1. Ensure timely reporting of suspected or confirmed cases of the disease to public health authorities as per local regulations.
  2. Facilitate contact-tracing activities by providing relevant information about the patient’s contacts and potential exposure sources.
  3. Collaborate with public health officials to implement control measures, such as quarantine or community outreach programs.
  4. Educate the patient and family members on the importance of disease notification and cooperation with public health authorities.
  5. Maintain the confidentiality and privacy of patient information while complying with reporting requirements.

Fluid Therapy:

  1. Assess the patient’s fluid status and electrolyte levels regularly to guide fluid therapy interventions.
  2. Administer intravenous fluids as prescribed, ensuring accurate calculations of fluid rates and electrolyte composition.
  3. Monitor the patient’s response to fluid therapy, including vital signs, urine output, and clinical signs of dehydration or fluid overload.
  4. Adjust the fluid therapy regimen based on ongoing assessment findings and the patient’s clinical status.
  5. Educate the patient and family members on the importance of fluid intake and adherence to the prescribed fluid therapy regimen.

Observation:

  1. Conduct frequent assessments of the patient’s vital signs, including temperature, pulse, respiratory rate, and blood pressure.
  2. Monitor the patient’s level of consciousness and mental status, noting any changes or signs of deterioration.
  3. Document intake and output accurately, including fluid intake, urine output, and any losses from vomiting or diarrhea.
  4. Perform regular physical assessments to monitor for signs of complications or deterioration in the patient’s condition.
  5. Communicate and collaborate with other members of the healthcare team to ensure comprehensive observation and monitoring of the patient.

Psychological Care:

  1. Provide emotional support and reassurance to the patient and family members, addressing fears and concerns about the disease and its treatment.
  2. Encourage open communication and active listening, allowing the patient to express their feelings and concerns.
  3. Offer information and education about the disease process, treatment options, and expected outcomes to alleviate anxiety and uncertainty.
  4. Facilitate access to pastoral care services or mental health support for patients experiencing emotional distress or psychological symptoms.
  5. Collaborate with the interdisciplinary team to develop and implement individualized care plans that address the patient’s psychosocial needs and promote coping strategies.

Hygiene:

  1. Assist the patient with personal hygiene activities, including bathing, oral care, and toileting, as needed.
  2. Ensure proper disposal of contaminated materials, such as soiled linens and medical waste, in accordance with infection control protocols.
  3. Educate the patient and family members on hand hygiene practices, including proper handwashing techniques and the use of hand sanitizer.
  4. Maintain a clean and sanitized patient care environment, including regular cleaning and disinfection of patient rooms and equipment.
  5. Implement standard precautions and transmission-based precautions as appropriate to prevent the spread of infection.

Nutrition:

  1. Assess the patient’s nutritional status and dietary intake, identifying any deficiencies or special dietary needs.
  2. Offer small, frequent meals and snacks that are easily digestible and well-tolerated by the patient.
  3. Encourage oral fluid intake to prevent dehydration, offering oral rehydration solutions or flavored beverages as tolerated.
  4. Collaborate with the dietitian to develop individualized meal plans that meet the patient’s nutritional requirements and preferences.
  5. Monitor the patient’s weight and nutritional status regularly, adjusting dietary interventions as needed to optimize nutritional intake and support recovery.

Advice for Home:

  1. Provide education and instructions on post-discharge care, including medication management, wound care, and follow-up appointments.
  2. Review signs and symptoms of complications or worsening illnesses that require prompt medical attention, such as persistent fever or difficulty breathing.
  3. Encourage the patient and family members to maintain good hygiene practices at home, including handwashing, surface cleaning, and proper food handling.
  4. Provide resources and referrals to community support services or home health agencies, if needed, to assist with ongoing care and support.
  5. Offer emotional support and encouragement to the patient and family members during the transition from hospital to home care, addressing any concerns or questions they may have.

Prevention and Control of Cholera:

  1. Proper Waste Disposal: Effective disposal and treatment of fecal waste contaminated with cholera bacteria, along with clothing and bedding that have come into contact with it, are paramount to preventing the spread of the disease.
  2. Sewage Management: Treatment of sewage before its discharge into waterways or underground water sources helps prevent potential undetected cholera patients from transmitting the disease through contaminated water.
  3. Source Protection: Posting warnings near contaminated water sources, along with guidelines on how to decontaminate water, helps alert individuals to the presence of cholera and mitigate the risk of infection.
  4. Water Sterilization: Boiling, filtering, and chlorinating water are effective methods for killing cholera bacteria and preventing the spread of infection. All materials that come into contact with cholera patients, including clothing and bedding, should be sterilized with hot water and, if possible, chlorine bleach. Hands and other body parts that touch cholera patients or their belongings should be thoroughly cleaned and sterilized. All water used for drinking, washing, or cooking should undergo sterilization by boiling or chlorination, especially in areas where cholera is prevalent.
  5. Improving Water Supply and Sanitation: Enhancing access to clean water and proper sanitation facilities helps reduce the risk of cholera transmission.
  6. Contact Tracing: Identifying and monitoring individuals who have come into contact with cholera patients helps prevent further spread of the disease.
  7. Personal Hygiene: Promoting good personal hygiene practices, such as regular handwashing, is essential for preventing cholera transmission.
  8. Postponing Festivals and Gatherings: Temporarily postponing large gatherings and festivals can help limit opportunities for cholera transmission in communities.
  9. Behavioral Changes: Encouraging behavioral changes, such as washing hands, boiling water, heating food before consumption, and using toilets or latrines, is crucial for preventing cholera infection.
  10. Adequate Case Treatment: Providing prompt and appropriate treatment to individuals diagnosed with cholera is vital for reducing morbidity and mortality associated with the disease.
  11. Active Case Reporting: Prompt reporting of suspected cholera cases in areas where the disease was previously not present facilitates early detection and intervention to prevent its spread.

Complications of Cholera:

  1. Paralytic Ileus: Cholera can lead to paralysis of the intestines, resulting in a condition known as paralytic ileus, which disrupts normal bowel function and can cause severe abdominal discomfort and distension.
  2. Muscle Weakness: Dehydration and electrolyte imbalances associated with cholera may lead to muscle weakness, which can affect mobility and overall physical strength.
  3. Cardiac Arrhythmias: Electrolyte disturbances, particularly potassium imbalances, can predispose individuals with cholera to develop irregular heart rhythms or cardiac arrhythmias, which may pose serious cardiac complications.
  4. Renal Failure: Severe dehydration and hypovolemia can compromise kidney function, leading to acute renal failure, characterized by a significant decrease in urine output and impaired kidney function.
  5. Metabolic Acidosis: Loss of bicarbonate ions through diarrhea and vomiting can result in metabolic acidosis, a condition characterized by an imbalance in the body’s acid-base equilibrium, leading to acidification of the blood and tissues.
  6. Hypoglycemia: Prolonged fasting and decreased oral intake in individuals with cholera can lead to low blood sugar levels, known as hypoglycemia, which may manifest as weakness, confusion, and even loss of consciousness if left untreated.
  7. Pulmonary Edema: In severe cases of cholera, fluid overload resulting from aggressive fluid resuscitation or electrolyte imbalances may lead to pulmonary edema, a condition characterized by the accumulation of fluid in the lungs, causing respiratory distress and compromised oxygenation.

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Dysentery | Causes | Pathophysiology | Signs and Symptoms | Nursing Management

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Dysentery is a well-known condition. It is characterized by the frequent passage of small, watery stools that often contain blood and mucus. This condition affects the large intestine and is accompanied by severe abdominal cramps. It can manifest as either an acute or chronic disease.

Causes of dysentery

Dysentery can be caused by various factors, including:

  1. Bacterial Infections: Pathogenic bacteria such as Shigella, Salmonella, Campylobacter, and Escherichia coli can cause dysentery through contamination of food or water sources.
  2. Parasitic Infections: Protozoa like Entamoeba histolytica can lead to dysentery when ingested through contaminated food or water.
  3. Viral Infections: Certain viruses, such as the norovirus, can cause dysentery-like symptoms, particularly in outbreaks or crowded environments.
  4. Poor Hygiene Practices: Inadequate sanitation, improper handwashing, and unsanitary living conditions can contribute to the spread of dysentery-causing pathogens.
  5. Contaminated Food and Water: Consumption of contaminated food or water, particularly in regions with inadequate sanitation, is a common cause of dysentery.
  6. Travel to Endemic Areas: Traveling to regions where dysentery is endemic increases the risk of exposure to the pathogens responsible for the condition.
  7. Weakened Immune System: Individuals with compromised immune systems, such as those with HIV/AIDS or undergoing immunosuppressive therapy, are more susceptible to developing dysentery.
  8. Poor Food Handling: Improper handling, storage, or preparation of food can lead to bacterial contamination and subsequent dysentery.

Types of dysentery

Dysentery is a term used to describe intestinal inflammation, particularly of the colon, resulting in severe diarrhea with blood and mucus in the feces. It is most commonly caused by bacterial or parasitic infections. There are two main types of dysentery:

  1. Bacterial Dysentery: This type of dysentery is caused by bacterial infections, most commonly by strains of bacteria such as:
    • Shigella: Shigellosis is caused by the Shigella bacteria and is a common cause of bacterial dysentery, especially in developing countries.
    • Campylobacter: Campylobacteriosis can also lead to dysentery-like symptoms, including bloody diarrhea.
    • Escherichia coli (E. coli): Certain strains of E. coli, such as E. coli O157:H7, can cause dysentery when ingested.
  2. Amoebic Dysentery: Amoebic dysentery is caused by the protozoan parasite Entamoeba histolytica. This type of dysentery is more common in tropical and subtropical regions and can lead to severe complications if left untreated.

Bacillary dysentery is a condition marked by acute inflammation and ulceration of the large intestine, manifesting as frequent small bowel movements containing blood and mucus in the stool. It is caused by non-motile gram-negative bacteria belonging to the genus Shigella. Shigella is classified into four strains:

  • Shigella flexneri,
  • Shigella boydii,
  • Shigella dysenteriae,
  • Shigella sonnei.

These types of dysentery share similar symptoms, including diarrhea, abdominal pain, fever, and sometimes dehydration. However, the treatment may vary depending on the specific cause, with bacterial dysentery often treated with antibiotics and amoebic dysentery treated with anti-parasitic medications. A proper diagnosis is essential for effective treatment.

Predisposing Factors

The predisposing factors contributing to the occurrence of dysentery can be summarized by the “6 F’s”: Formites, Food, Faeces, Fingers, Fluids, and Flies. Addressing these factors effectively can help mitigate the problem. These factors include:

i. Poor feeding practices: This encompasses the improper handling of feeding bottles for infants, which may become contaminated if not cleaned adequately. Additionally, consuming unboiled or improperly prepared foods increases the risk of dysentery transmission.

ii. Inadequate personal hygiene: This involves insufficient attention to hand hygiene, such as inadequate handwashing practices and neglecting to trim and maintain fingernails. Poor personal hygiene can facilitate the transmission of pathogens responsible for dysentery.

iii. Unsafe water sources and storage: The lack of access to safe drinking water, coupled with inadequate treatment and storage facilities, can expose individuals to waterborne pathogens, including those causing dysentery.

iv. Inadequate sanitation: This encompasses issues such as the presence of rubbish pits or dumping sites in close proximity to living areas, as well as poorly maintained sewerage lines. These conditions create environments conducive to the proliferation and spread of disease-causing organisms.

v. Overcrowding: Overcrowded living conditions facilitate the rapid spread of infectious diseases like dysentery. Close contact between individuals increases the likelihood of transmission, particularly in settings where sanitation and hygiene practices are suboptimal.

Epidermiology

Bacillary dysentery is predominantly found in unhygienic tropical regions; however, due to its ease of transmission, sporadic outbreaks can occur worldwide. The disease is particularly prevalent among densely populated communities, including nursing homes and large institutions where overcrowding is common.

Mode of Transmission 

When examining this picture, one immediately thinks about the mode of transmission of dysentery. Shigella, the causative agent, spreads primarily through the fecal-oral route. The bacteria are expelled in feces, and inadequate sanitation and hygiene practices can lead to contamination of food and water sources. Flies further exacerbate the problem by frequently spreading the bacteria to food, making them a significant mode of transmission for dysentery. Figure 8 depicts the transmission pathway of dysentery, highlighting the importance of proper sanitation and hygiene measures in preventing its spread. The incubation period of Shigella is typically 1 to 7 days.

Pathophysiology

Dysentery, particularly bacillary dysentery caused by Shigella species, involves a complex series of events within the gastrointestinal tract. It begins with the ingestion of Shigella bacteria, often through contaminated food, water, or contact with infected individuals. Upon reaching the lower intestine, Shigella bacteria adhere to and invade the epithelial cells lining the intestinal mucosa. This invasion triggers a vigorous inflammatory response characterized by the release of pro-inflammatory cytokines and chemokines, recruiting immune cells such as neutrophils and macrophages to the site of infection.

As Shigella infiltrates the intestinal tissue, it causes damage to the epithelial cells, disrupting the mucosal barrier. This damage facilitates the release of toxins produced by Shigella species, including Shiga toxin, which further exacerbates tissue damage and inflammation. Consequently, mucosal ulceration occurs in the colon, resulting in the formation of erosions or ulcers in the intestinal lining. These ulcers contribute to the hallmark symptoms of dysentery, such as abdominal pain, cramping, frequent and urgent bowel movements, and the passage of bloody and mucoid stools.

In severe cases, dysentery can lead to complications such as dehydration due to fluid loss from diarrhea, electrolyte imbalances, systemic spread of infection leading to sepsis, and, rarely, the development of conditions like reactive arthritis or hemolytic uremic syndrome (HUS). Overall, understanding the pathophysiology of dysentery is crucial for the development of effective prevention strategies and treatments aimed at mitigating the impact of this infectious disease on affected individuals and communities.

Signs and Symptoms

  • Dysentery presents with a sudden onset of symptoms.
  • Fever is common due to infection and inflammation.
  • Dehydration signs, like loss of skin turgor, may occur due to diarrhea; however, dehydration may not always be present as stool frequency increases.
  • Abdominal discomfort is an early symptom, likely from irritation of the gastrointestinal tract’s mucosal lining by the bacteria.
  • Nausea and vomiting may result from irritation of the stomach’s mucosal lining.
  • Colicky abdominal pains are common, likely due to the inflammatory reaction in the intestinal mucosal lining.
  • Bloody diarrhea is characteristic, resulting from damage to the large intestine’s mucosal lining during inflammation, potentially damaging capillaries.
  • Bloody diarrhea often accompanies urgency and tenesmus, with urgency being the frequent urge to defecate even with small stool amounts passed, and tenesmus being the painful, ineffective straining to empty the bowels.

Management:

  1. Correct electrolyte and fluid imbalance.
  2. Eliminate the causative organism.
  3. Prevent and manage complications.

Investigations:

  • Microscopic examination of a fresh stool specimen and rectal swab for culture and sensitivity. Stool should be cultured promptly after collection. Detection of the organism in stool confirms diagnosis.
  • Immunofluorescent techniques can be used to detect the organism in stool.
  • Sigmoidoscopy can reveal a red, bleeding mucosa with patches of necrotic membrane, which may separate to leave ulcerated areas.

Therapy:

Fluid and electrolyte replacement: Oral rehydration is typically necessary to address fluid and electrolyte imbalances. However, each patient should undergo assessment to determine the extent of dehydration and receive appropriate fluid replacement therapy.

Drugs: Antibiotics are prescribed to shorten the duration of illness and prevent relapse. Any of the following antibiotics can be given while awaiting the results of culture and sensitivity:

  • Nalidixic acid: 1g orally four times a day for 7 to 14 days.
  • Ciprofloxacin: 500mg orally twice daily for 5 days.
  • Trimethoprim-Sulfamethoxazole (Septrin, Co-trimoxazole): 960mg orally twice daily for 5 days.
  • Chloramphenicol: 50 to 100mg per kilogram of body weight orally four times a day for 5 days.
  • Ampicillin: 500mg orally four times a day for 5 days.

Amoebic dysentery

Amoebic dysentery, also known as amoebiasis, is the second type of dysentery caused by an infection with the pathogenic amoeba Entamoeba histolytica. This chronic enteric infection is brought about by a protozoan organism known as Entamoeba histolytica, which is a single-celled parasite.

  • Cause: Amoebic dysentery is caused by the protozoan parasite Entamoeba histolytica.
  • Predisposing Factors: Similar to bacillary dysentery, predisposing factors include poor sanitation, inadequate hygiene practices, contaminated food and water sources, overcrowding, and low socioeconomic conditions.
  • Epidemiology: Entamoeba histolytica has a global distribution and is endemic in regions with poor sanitation and low socioeconomic status. The use of night soil (human feces used as fertilizer) in agriculture facilitates the spread of the disease. The organism is acquired through the ingestion of cysts.
  • Mode of Transmission: Transmission occurs primarily through the fecal-oral route, where ingestion of contaminated food or water containing cysts leads to infection. Vectors such as flies, cockroaches, and rodents can carry cysts and contaminate food and drink, further spreading the disease.
  • Incubation Period: The incubation period for amoebic dysentery can vary widely, ranging from 2 weeks to years. Human beings serve as the principal reservoirs and carriers of the parasite, contributing to its transmission.

Pathophysiology:

When ingested, cysts of Entamoeba histolytica enter the alimentary tract via the mouth and proceed to the stomach, where they undergo excystation during digestion. Motile trophozoites are released, which then multiply. These trophozoites proceed to invade and ulcerate the intestinal mucosa of the large bowels, forming flask-like ulcers. Additionally, some of the amoebae may travel through the mesenteric artery, reaching the liver. In the liver, they cause total destruction, resulting in amoebic hepatocellular necrosis and the formation of liver abscesses.

Signs and Symptoms:

  • The onset of symptoms is gradual and typically involves abdominal discomfort.
  • Other signs and symptoms may include:
    • Mildly loose stools or frank diarrhea, sometimes with blood and mucus. Diarrhea may alternate with episodes of constipation.
    • Tenderness may develop over the caecum, transverse colon, or sigmoid.
    • Fever may be present.
    • Abdominal pains that may occur intermittently.
    • In cases of hepatic amoebiasis, symptoms may include body malaise, fluctuating temperature, sweating, and an enlarged, tender liver.
    • Foul-smelling stool.
    • Weight loss in chronic cases.

Investigations:

  • Stool microscopy, culture, and sensitivity testing (m/c/s) can help identify the presence of Entamoeba histolytica.
  • History of blood-stained stool is essential for diagnosis.
  • Physical examination may reveal signs of dehydration.
  • Rectal swab culture can aid in confirming the presence of the parasite.
  • Hemoglobin (Hb) levels in blood can indicate anemia, which may occur due to chronic infection.
  • Sigmoidoscopy can visualize ulcers in the intestinal mucosa.
  • Liver scan may be conducted to detect liver abscesses.

Treatment:

The disease is managed with the following interventions:

  • Flagyl (metronidazole) at doses of 200-400mg three times daily.
  • Septrin (trimethoprim-sulfamethoxazole) at a dose of 960mg twice daily for 5-7 days.
  • Furamide (diloxanide furoate) at a dose of 500mg three times daily for 10 days.
  • For hepatic amoebiasis, Flagyl (metronidazole) and Chloroquine are given at a dose of 600mg once daily for 2 days, followed by 300mg once daily for 21 days.
  • Panadol (acetaminophen) may be prescribed for fever and pain relief.
  • Intravenous fluids, such as Ringer’s lactate, may be administered to manage dehydration.

Nursing Care of Dysentery:

The goals of nursing care include:

  • Preventing further transmission of infection.
  • Replenishing lost fluids and electrolytes.
  • Preventing complications such as shock.

Environment:

  • Admit the patient to an isolation room separate from other patients to prevent the spread of infection. The room should be well-lit for easy observation and have good ventilation to promote air circulation. Position the patient near the toilet for convenience. Ensure essential equipment such as drip stands, intravenous sets, and observation trays are readily accessible within the patient’s environment.

Observation:

  • Monitor the patient’s general condition regularly. Frequently monitor vital signs such as temperature, pulse, respiration, and blood pressure. The frequency of observations depends on the patient’s condition. Assess the quality and quantity of stool passed by the patient. Monitor intake and output and record on fluid balance charts. Evaluate stool characteristics including amount, consistency, and color, and report any abnormalities. Watch for signs of dehydration such as loss of skin elasticity, sunken eyes, thirst, and dry mucous membranes of the mouth.

Infection Prevention:

  • Isolate the patient away from other patients to prevent the spread of infection. Individuals coming into contact with the patient should adhere to isolation protocols, including wearing gowns and masks when entering the room and washing hands before and after attending to the patient. Limit visitors to reduce the risk of infection transmission. Disinfect patient linens with a solution of JIK 1:6 and label them as “infectious” before sending them to the laundry. Avoid mixing this linen with other ward linens. Administer prescribed medication to treat the causative organism. Disinfect all utensils used by the patient to prevent contamination and further spread of infection.

Nutrition:

Provide the patient with plenty of fluids to ensure hydration, along with a gentle diet that is free from irritants. If the patient is unable to consume food or fluids orally due to their condition, initiate intravenous fluid therapy to maintain hydration and electrolyte balance. It’s essential to closely monitor both the intake and output of fluids. Keep detailed records of the amount and type of fluids administered intravenously, noting the start time of IV fluid therapy and the date it commenced. Additionally, record the patient’s oral intake and output to accurately assess their fluid balance and nutritional status.

Hygiene:

Depending on the patient’s condition, offer assistance with a bed bath to enhance comfort, preserve self-esteem, and eliminate dirt. Provide oral care assistance to prevent complications arising from poor oral hygiene, such as mouth infections. This also aids in promoting salivation, particularly crucial when the patient experiences dry mouth due to significant fluid loss. Promptly change soiled linens as needed, ensuring they are disinfected with a solution of Jik 1:6 before being sent to the laundry. This helps maintain cleanliness and reduce the risk of infection. Thoroughly clean the perineal area to uphold hygiene standards and minimize the risk of infections in this sensitive region.

Psychological Care:

Patients with dysentery may experience feelings of neglect, therefore, it’s essential for nurses to provide appropriate psychological support to alleviate anxiety. Educate the patient about the disease process, including its cause, mode of transmission, signs and symptoms, treatment, and potential complications. Explain the necessity of isolation to the patient, emphasizing its role in preventing the spread of infection. Similarly, inform significant others why visitation is restricted. Ensure that any procedures performed on the patient are thoroughly explained to gain their cooperation. Encourage patients to ask questions, and respond truthfully to address their concerns. This fosters trust and understanding between the patient and healthcare provider.

Medication Management:

Administer medications as prescribed by the healthcare provider, ensuring adherence to dosage and timing instructions. Monitor the patient closely for any adverse reactions or side effects that may occur as a result of medication administration. Additionally, administer fluids to the patient based on their individual condition and hydration status. Adjust fluid administration according to the patient’s fluid balance and response to treatment. Regularly assess the patient’s response to both medication and fluid therapy, and promptly report any concerning symptoms or changes in condition to the healthcare team. This proactive approach helps to ensure effective management of dysentery and promotes optimal patient outcomes.

Elimination Management:

Monitor and record the patient’s intake and output meticulously to track fluid balance and hydration status accurately. Observe stool characteristics, including volume, consistency, contents, and odor, to assess gastrointestinal function and identify any abnormalities. Initially, provide a bedpan for elimination, ensuring patient comfort and dignity. As the patient’s condition improves, encourage and assist them to use the toilet independently. This gradual transition promotes patient mobility and autonomy while maintaining hygiene and minimizing discomfort.

Prevention and Control of Dysentery:

Based on our discussion regarding the mode of transmission and predisposing factors of dysentery, several measures can be implemented to prevent its occurrence:

  1. Improved Environmental Sanitation: This includes:
  • Providing safe and sufficient water supply to communities.
  • Ensuring the safe and proper disposal of human waste through the use of pit latrines or toilets.
  • Implementing measures to safeguard food against fecal contamination.
  • Offering information, education, and communication campaigns about dysentery to raise awareness and promote preventive measures.
  • Discouraging the use of untreated human waste as fertilizer or manure, which can contribute to the spread of the disease.

Early Diagnosis and Treatment of Cases and Carriers:

  • Ensure prompt detection and provide appropriate and adequate treatment for both cases and carriers of dysentery.
  • Conduct regular screening of food handlers to identify and prevent potential sources of infection.

Improved Personal and Communal Hygiene:

  • Encourage adequate handwashing with soap and running water after using the toilet and before handling or consuming food.
  • Promote the use of pit latrines or toilets for defecation to prevent fecal contamination of the environment.
  • Prohibit children from defecating on the ground; instead, use toilet training pots and disinfect them after each use. Dispose of children’s stools in the toilet or pit latrine.
  • Boil water for drinking and washing vegetables and fruits to eliminate potential sources of contamination.
  • Avoid consuming vegetable and fruit salads, which may pose a risk of transmitting infection if not properly washed or cooked.

Complications of Dysentery:

  1. Perforation of the colon due to ulceration: Ulcers formed in the colon may lead to perforation, allowing the contents of the colon to spill into the abdominal cavity.
  2. Peritonitis due to perforation: If the colon perforates, the resulting spillage of intestinal contents can cause peritonitis, leading to severe abdominal inflammation and infection.
  3. Rectal prolapse due to tenesmus: Persistent straining during bowel movements (tenesmus) can lead to rectal prolapse, where the rectum protrudes through the anus.
  4. Hematogenous dissemination of the Shigella bacteria (rare): In some cases, Shigella bacteria may spread through the bloodstream, causing abscesses in various organs and potentially leading to meningitis.
  5. Acute, nonsuppurative arthritis: Large weight-bearing joints may become inflamed during the recovery phase, resulting in acute arthritis.
  6. Conjunctivitis, iritis, and peripheral neuropathy (rare): Rare complications may include inflammation of the eyes (conjunctivitis and iritis) and damage to peripheral nerves.
  7. Hemolytic uremic syndrome (7-10 days after onset): A severe complication characterized by acute kidney failure, low platelet count, and red blood cell breakdown.
  8. Toxic megacolon: The colon may become massively dilated due to inflammation, leading to life-threatening complications.
  9. Hemiplegia: In rare cases, dysentery may lead to paralysis affecting one side of the body (hemiplegia).
  10. Encephalopathy: Severe dysentery can cause brain dysfunction, leading to encephalopathy and neurological symptoms.
  11. Septicemia: The presence of pathogens in the bloodstream can lead to systemic infection and septicemia.
  12. Hyponatremia: Imbalances in electrolytes, such as low sodium levels, may occur due to excessive dehydration from diarrhea.
  13. Reiter’s syndrome: A reactive arthritis that can develop following an infection, characterized by joint pain, eye inflammation, and urinary tract symptoms.
  14. Liver abscess: Shigella infection may lead to the formation of abscesses in the liver, causing abdominal pain and other symptoms.
  15. Renal failure: Severe dehydration resulting from dysentery can lead to kidney failure due to reduced blood flow and electrolyte imbalances.

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Crohn’s Disease | Causes | Pathophysiology | Nursing Management

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Crohn’s disease is a chronic inflammatory condition of the gastrointestinal system, primarily impacting the distal ileum and colon. However, it can also affect any part of the digestive tract, from the mouth to the anus. This disorder is characterized by nonspecific inflammation, and its exact cause remains unknown. Crohn’s disease manifests as an idiopathic inflammatory process that can involve any segment of the gastrointestinal tract.

Epidemiology

Crohn’s disease can develop at any age, but it most commonly occurs between 25 and 30 years old. Both men and women are affected, with a slightly higher incidence among women. One-third of cases primarily involve the small bowel, often affecting the terminal ileum (ileitis). Approximately half of cases involve both the small bowel and colon, with the terminal ileum and adjacent proximal ascending colon being most commonly affected (ileocolitis). In 15-20% of cases, only the colon is affected.

Causes

The exact cause of Crohn’s disease remains unknown, but it is associated with several factors:

  • Genetic Factors: Crohn’s disease can have a familial predisposition, with certain genes inherited from parents increasing the risk of developing the condition.
  • Immune Disorders: Inflammation in Crohn’s disease may result from immune system dysfunction, leading it to mistakenly attack the normal flora of the gastrointestinal tract.
  • Previous Infection: Prior infections may trigger an abnormal immune response, contributing to the development of Crohn’s disease.
  • Smoking: Smokers with Crohn’s disease typically experience more severe symptoms compared to non-smokers.

Pathophysiology

Crohn’s disease can affect any part of the gastrointestinal (GI) tract, but it is most commonly observed in the terminal ileum, jejunum, and colon. The inflammation extends through all layers of the bowel wall (transmural). Typically, affected areas are not continuous, with segments of normal bowel interspersed between diseased portions. Ulcerations in Crohn’s disease are often deep and longitudinal, penetrating between islands of inflamed, edematous mucosa, resulting in the characteristic cobblestone appearance. Thickening of the bowel wall and narrowing of the lumen occur, leading to the development of strictures. Additionally, abscesses or fistula tracts may form, connecting with other loops of the bowel, skin, bladder, rectum, or vagina.

Clinical Manifestations

The manifestations of Crohn’s disease depend primarily on:

  • The anatomical site of involvement
  • The extent of the disease process
  • The presence or absence of complications

Common symptoms include:

  • Crampy abdominal pains caused by the intestines’ inability to transport gastrointestinal products through constricted lumens.
  • Chronic diarrhea resulting from continuous irritating discharge emptied into the colon from swollen intestines, often accompanied by blood.
  • Weight loss due to malabsorption and reduced food intake.
  • Fever, indicating infection.
  • Nausea and vomiting, which may signal the onset of small bowel obstruction.
  • Constipation: While most patients experience diarrhea, some may suffer from constipation due to inflammation around the anus, making defecation difficult.

Management

Aims

  1. Control the inflammatory process.
  2. Relieve symptoms.
  3. Correct metabolic and nutritional problems and promote healing.

Diagnostic Studies

  • Proctosigmoidoscopy: is typically the initial procedure to assess inflammation in the rectosigmoid area.
  • Stool Occult Blood Test.
  • Barium Enema: useful for identifying strictures and fissures.
  • Small Bowel X-ray: Can reveal irregular mucosa, ulcerations, and stiffening.
  • Sigmoidoscopy and colononoscopy: These procedures show patchy areas of inflammation.
  • Biopsy: Obtained during sigmoidoscopy, it reveals granulomatous tissue.
  • Blood tests: These may demonstrate an increased white blood cell count, a reduced erythrocyte sedimentation rate (ESR), and a decreased hemoglobin level.

Drug Therapy

While there is no specific therapy for Crohn’s disease, the following drugs may help manage symptoms:

  1. Corticosteroids (e.g., Prednisolone):
    • Dosage: Prednisolone 5–60 mg daily orally, given as a single dose or in divided doses. The maximum daily dose is 250mg.
    • Mode of Action: stimulates the synthesis of enzymes to decrease the inflammatory response.
    • Side Effects: suppression of the immune system, resulting in lymphocytopenia.
  2. Aminosalicylates (e.g., Sulfasalazine):
    • Dosage: Initial 3–4 g orally daily in divided doses, followed by a maintenance dose of 2g orally daily in divided doses.
    • Mode of Action: Believed to be metabolized by intestinal flora in the colon, producing anti-inflammatory and antibacterial effects.
    • Side Effects: reduced appetite, stomatitis, vertigo.
  3. Antibiotics (e.g., Metronidazole):
    • Dosage: 200–400 mg orally three times daily for 7–10 days.
    • Mode of Action: Bactericidal action by inhibiting bacterial DNA synthesis.
    • Side Effects: dry mucous membranes, metallic taste.
  4. Anti-Diarrheals (e.g., Loperamide):
    • Dosage: 4mg initially orally, then 2mg per loose stool. The maximum dose is 16mg in 24 hours.
    • Mode of Action: Reduces intestinal motility and fluid secretion.
    • Side Effects: constipation, abdominal pain, dry mouth, drowsiness.
  5. Analgesics (e.g., Paracetamol):
    • Dosage: 500–1000 mg orally three times daily.
    • Mode of Action: non-narcotic analgesic, antipyretic, and anti-inflammatory.
    • Side Effects: Rare, but may include nausea, vomiting, and liver damage.

Other measures include:

  • Vitamin supplements address the bowel’s inability to absorb nutrients effectively.
  • In severe cases, patients may need to abstain from oral intake and receive parenteral feeds.
  • Surgery may be necessary for severe cases, which may involve:
    • Removing the affected portion of the bowel.
    • Repairing fistulas.
    • Draining abscesses.

Nursing Care Environment:

  1. Observation in the Acute Bay:
    • Place the patient in the acute bay for close monitoring and easy observation by nursing staff.
    • Ensure the bay is equipped with necessary monitoring equipment and resources for prompt intervention if needed.
  2. Well-Ventilated Environment:
    • Maintain a well-ventilated environment to eliminate odors and promote comfort for the patient.
    • Ensure adequate airflow to prevent the buildup of airborne pathogens and maintain a hygienic environment.
  3. Rest Promotion:
    • Create a quiet and calm environment to facilitate rest and relaxation for the patient.
    • Coordinate nursing activities to minimize disturbances and interruptions, allowing the patient to rest uninterrupted.
    • Administer prescribed analgesics as needed to alleviate pain and discomfort, promoting restful sleep and overall comfort.
  4. Pain Management:
    • Assess the patient’s pain levels regularly and administer analgesics as prescribed to manage pain effectively.
    • Utilize non-pharmacological pain management techniques such as positioning, relaxation techniques, and heat therapy to complement medication therapy.
    • Monitor the patient for any adverse reactions or side effects of analgesic medications, and intervene promptly as needed.
  5. Hygiene and Comfort:
    • Maintain the patient’s personal hygiene by assisting with activities of daily living such as bathing, oral care, and changing bed linens.
    • Ensure the patient’s comfort by providing appropriate bedding, adjusting room temperature, and addressing any discomfort promptly.
    • Encourage adequate hydration and nutrition to support the patient’s overall well-being and recovery.
  6. Emotional Support:
    • Offer emotional support and reassurance to alleviate anxiety and promote a sense of security for the patient.
    • Provide opportunities for the patient to express concerns and feelings and validate their emotions in a supportive manner.
    • Collaborate with the interdisciplinary team to address any psychosocial needs or concerns identified during care provision.

Observations:

  1. Assessment of General Condition:
    • Regularly assess the patient’s overall condition to determine improvement or deterioration.
    • Monitor for changes in consciousness, level of alertness, and response to treatment interventions.
  2. Vital Signs Monitoring:
    • Check vital signs frequently, with the frequency based on the patient’s condition (e.g., every two or four hours).
    • Monitor temperature, blood pressure, heart rate, and respiratory rate to identify any abnormalities or signs of deterioration.
  3. Fluid Intake and Output Monitoring:
    • Monitor the intake and output of fluids, including both oral and intravenous fluids.
    • Watch for signs of dehydration or fluid overload, which can lead to complications such as renal failure.
  4. Assessment of Vomitus and Stool:
    • Observe the consistency, color, and amount of vomitus and stool.
    • Changes in these parameters may indicate changes in the patient’s condition or potential complications.
  5. Drug Side Effects Monitoring:
    • Monitor for side effects of prescribed medications, such as corticosteroids or antibiotics.
    • Be vigilant for adverse reactions, and promptly report any concerns to the healthcare team.
  6. Observation for disease complications:
    • Watch for complications of the disease, such as abdominal distension, which may indicate intestinal obstruction.
    • Assess for signs of complications and report any findings promptly for further evaluation and management.

Medication Administration:

  1. Administer prescribed medications:
    • Ensure timely administration of prescribed medications, such as Metronidazole, as directed by the healthcare provider’s orders.
    • Follow appropriate medication administration protocols and double-check dosage and route to prevent errors.
  2. Monitoring for side effects:
    • Vigilantly observe the patient for any potential side effects or adverse reactions associated with the medication.
    • Educate the patient about common side effects to watch for and report any new or worsening symptoms promptly.
  3. Documentation:
    • Document medication administration accurately and thoroughly in the patient’s medical record, including the medication name, dosage, route, and time administered.
    • Record any observed side effects or adverse reactions, as well as any interventions implemented in response.
  4. Patient Education:
    • Provide patient education regarding the purpose of the medication, its potential side effects, and the importance of adherence to the prescribed regimen.
    • Encourage the patient to ask questions and express any concerns about their medication therapy.
  5. Collaboration with the Healthcare Team:
    • Collaborate with the healthcare team to monitor the patient’s response to medication therapy and adjust the treatment plan as needed.
    • Communicate any significant findings or concerns related to medication side effects promptly to the healthcare provider for further evaluation and management.
  6. Follow-Up:
    • Schedule follow-up assessments to monitor the patient’s response to medication therapy and evaluate for any ongoing or new side effects.
    • Continuously reassess the patient’s medication needs and make recommendations for adjustments as necessary to optimize therapeutic outcomes.me

Psychological Care:

  1. Patient and Family Education:
    • Explain the disease process comprehensively to the patient and their family, ensuring they understand the condition.
    • Provide information on the causes, signs, symptoms, and available treatment options to empower them with knowledge.
  2. Emphasize Treatment Compliance:
    • Inform the patient that the effectiveness of treatment hinges on their adherence to prescribed medication regimens.
    • Stress the importance of following the treatment plan as directed by healthcare professionals to achieve optimal outcomes.
  3. Emotional Support:
    • Offer empathetic support to both the patient and their family members to alleviate anxiety and address concerns.
    • Encourage open communication and reassure the patient that their feelings and questions are valued and will be addressed with honesty and compassion.
  4. Establish Rapport:
    • Foster a trusting relationship by actively listening, maintaining a calm demeanor, and exuding confidence in providing care.
    • Be attentive to the patient’s needs and concerns, demonstrating empathy and understanding throughout interactions.
  5. Addressing Questions:
    • Respond to the patient’s questions promptly and truthfully, providing accurate information to build confidence in the treatment plan.
    • Encourage ongoing dialogue and offer reassurance that the healthcare team is available to address any uncertainties or worries.

Hygiene Care:

  1. Bathing:
    • Ensure regular bathing to promote blood circulation and maintain overall cleanliness and comfort for the patient.
    • Use appropriate hygiene products and techniques to gently cleanse the skin while minimizing irritation.
  2. Oral Care:
    • Implement thorough oral care practices to promote salivation, prevent halitosis, and reduce the risk of mouth infections.
    • Encourage regular brushing and flossing of teeth, as well as the use of mouthwash, as appropriate.
    • Provide assistance with oral care procedures as needed to ensure proper hygiene.
  3. Skin Care:
    • After each bowel movement, provide meticulous skin care to prevent irritation and infection.
    • Cleanse the perianal area gently with mild soap and water, patting dry afterward to avoid friction and skin breakdown.
    • Apply protective ointments or barrier creams as indicated to soothe and protect the skin from irritation.

Nutrition and Fluids:

  1. Dietary Provision:
    • Offer a diet rich in proteins to facilitate tissue repair and carbohydrates to supply energy, along with essential vitamins to support immunity.
    • In cases of severe illness, consider parenteral nutrition to provide essential nutrients directly into the bloodstream.
  2. Meal Frequency:
    • Provide meals in small, frequent portions rather than larger amounts to minimize the risk of vomiting and promote better tolerance.
    • Offer nutrient-dense snacks between meals to maintain energy levels and support nutritional intake throughout the day.
  3. Fluid Encouragement:
    • Encourage the patient to increase fluid intake to maintain hydration and support overall health.
    • Offer a variety of beverages, including water, clear soups, and electrolyte-rich drinks, to prevent dehydration and promote hydration.

Elimination Care:

  1. Bedpan Use:
    • Initially, provide bedpans for patients who are unable to ambulate to the toilet due to illness or weakness.
    • As the patient’s condition improves, encourage mobility and assist them in using the toilet as appropriate.
  2. Toilet Assistance:
    • As the patient becomes more mobile and independent, position them near the toilet to facilitate regular toileting.
    • Provide necessary assistance and support as needed to ensure safe and comfortable elimination.
  3. Stool Observation:
    • Regularly observe the stool for consistency, amount, and odor to monitor gastrointestinal health and assess for any abnormalities.
    • Document any significant changes in stool characteristics and report findings to the healthcare team for further evaluation if necessary.

Patient Education:

  1. Disease Education:
    • Educate the patient about their condition, including the signs, symptoms, and potential complications associated with it.
    • Provide information on how the disease may progress and what to watch for in terms of worsening symptoms.
  2. Importance of Rest:
    • Emphasize the significance of rest in managing the condition, explaining that limiting physical activity can reduce intestinal motility and support healing.
    • Encourage the patient to prioritize rest and avoid overexertion to prevent exacerbating symptoms.
  3. Drug Compliance:
    • Stress the importance of adhering to prescribed medication regimens to effectively manage symptoms and prevent disease progression.
    • Educate the patient about the potential consequences of non-compliance and the importance of taking medications as directed by healthcare providers.
  4. Follow-Up Appointments:
    • Explain the importance of attending scheduled follow-up appointments as directed by healthcare providers.
    • Emphasize the role of regular monitoring in assessing disease status, adjusting treatment plans, and preventing complications.
  5. Nutritional Importance:
    • Teach the patient about the significance of maintaining a well-balanced diet to support overall health and manage the condition effectively.
    • Provide guidance on dietary choices that promote healing and minimize symptoms, such as consuming adequate protein, fiber, and hydration.

Complications:

  1. Abscess:
    • Symptoms include a tender abdominal mass, fever, and leukocytosis, indicating the presence of an abscess.
    • Treatment involves broad-spectrum antibiotics and, if malnourished, Total parental nutrition (TPN).
    • Percutaneous drainage or surgery may be necessary for resolution.
  2. Obstruction:
    • Small bowel obstruction can result from active inflammation or chronic fibrotic stricture formation, often exacerbated by dietary indiscretion.
  3. Fistulas:
    • Enteromesenteric and enteroenteric fistulas are often asymptomatic, but may lead to complications such as abscess formation or bowel obstruction.
  4. Perianal Disease:
    • Patients with fissures, fistulas, and skin tags may experience perianal discomfort.
    • Conservative management includes sitz baths and the use of cotton pads to absorb drainage.
  5. Carcinoma:
    • Patients with colonic Crohn’s disease are at increased risk of developing colon carcinoma.
    • Some authorities recommend screening colonoscopies for early detection and intervention.
  6. Hemorrhage:
    • Unlike ulcerative colitis, severe hemorrhage is uncommon in Crohn’s disease.
  7. Malabsorption:
    • Malabsorption can arise from bacterial overgrowth, strictures, jejunal inflammation, or surgical resections.
    • Management involves addressing underlying causes and optimizing nutritional support to mitigate complications.

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Malabsorption Syndrome | Etiology, Nursing Care Management

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Introduction

Malabsorption syndrome refers to a group of disorders characterized by the inability of the digestive system to properly absorb nutrients from food. This can lead to deficiencies in essential vitamins, minerals, and other nutrients, causing various symptoms and complications. Common causes include gastrointestinal diseases such as celiac disease, Crohn’s disease, and pancreatic insufficiency. Symptoms may include diarrhea, weight loss, fatigue, and nutritional deficiencies. Treatment typically involves addressing the underlying cause and managing symptoms through dietary changes, supplements, and medication.

Etiology

The root cause of malabsorption syndrome lies in the inadequate absorption of essential nutrients due to various diseases. This can stem from issues in digestion, where nutrients aren’t properly broken down for absorption, or from difficulties in transporting digested nutrients across the brush border of the intestinal villi.

Diseases contributing to malabsorption include:

  1. Celiac disease
  2. Dermatitis herpetiformis
  3. Tropical sprue
  4. Bacterial overgrowth
  5. Whipple’s disease (resulting in villi growth impairment)
  6. Short-bowel syndrome
  7. Lactase deficiency
  8. Parasitic infestations like Giardia intestinalis.

The classification

The classification of malaasorption syndrome involves categorizing it based on the underlying causes and mechanisms. It can be broadly classified into two main types:

  1. Primary Malabsorption: This type occurs due to intrinsic defects within the digestive system, such as enzyme deficiencies or structural abnormalities in the intestinal lining. Examples include:
    • Celiac disease
    • Dermatitis herpetiformis
    • Short-bowel syndrome
  2. Secondary Malabsorption: This type is secondary to other medical conditions or factors that affect the absorption process, such as inflammation, infection, or surgical interventions. Examples include:
    • Tropical sprue
    • Bacterial overgrowth
    • Whipple’s disease
    • Lactase deficiency
    • Parasitic infestations, like Giardia intestinalis

Clinical Manifestations

Patients admitted to the hospital with malabsorption may present with the following features:

  1. Steatorrhea: excretion of more than 7g of fat daily in feces. Stools are typically pale, bulky, foul-smelling, and difficult to flush.
  2. Wasting: Failure to absorb essential nutrients leads to muscle wasting and weight loss. However, weight loss may not be apparent due to ascites and/or edema.
  3. Abdominal Distension: Increased bulk of intestinal contents and gas production can cause abdominal distension, accompanied by borborygmi (audible bowel sounds) and flatulence. Patients may experience abdominal discomfort.

Signs and Symptoms

Signs and Symptoms of Specific Deficiencies in Malabsorption:

  1. Fatigue: resulting from anemia and/or hypokalemia.
  2. Edema: due to hypoproteinemia and/or anemia.
  3. Tetany: caused by hypocalcemia.
  4. Hemorrhage: manifested as ecchymosis or purpura due to vitamin K deficiency.
  5. Anemia: results from iron deficiency.
  6. Decreased Libido.
  7. Glossitis and stomatitis result from deficiencies in folic acid and vitamin B.
  8. Bone Conditions: include osteoporosis, osteomalacia, and bone pain due to hypocalcemia and vitamin D deficiency.
  9. Increased Susceptibility to Infections: Due to globulin deficiency.
  10. Pigmentation of Skin and Mucous Membranes: Resulting from Hypoadrenalism.
  11. Hypotension, hypothermia, and inhibition of growth: due to depression of endocrine activity.
  12. Mental changes are particularly observed in gluten enteropathy.

Diagnosis

  1. Stool Analysis: Checking for bacterial growth and parasites, such as isolating Giardia lamblia cysts.
  2. Jejunal Biopsy: Obtaining mucosal samples via jejunoscopy to assess for malignancy or villi atrophy.
  3. Radiological Tests:
    • Ultrasound Scan
    • Computed Tomography (CT) Scan
    • Magnetic Resonance Imaging (MRI)
    • Barium Meal: Revealing dilation, segmentation, and loss of normal appearance in the small intestine, particularly the jejunum.
  4. Complete Blood Cell Count (CBC): To screen for anemia.
  5. Ultrasound Scan: May detect pancreatic or intestinal tumors.

Medical and Nursing Management

  1. Address the underlying cause: Treat or remove the primary cause, such as implementing a gluten-free diet for celiac disease or administering pancreatic extract for chronic pancreatic disease. Antibiotic therapy may be needed for conditions like diverticulosis.
  2. Compensate for malabsorption: In cases where specific treatment is not feasible, like after extensive stomach or intestine resections, focus on increasing the intake of essential nutrients and calories to overcome malabsorption.
  3. Correct deficiencies: Replace specific deficiencies identified through intravenous therapy when necessary to ensure proper nutrient levels.
  4. Alleviate symptoms: Implement strategies to reduce symptoms associated with steatorrhea, such as dietary modifications or medication.

Drugs

The medications prescribed for patients with malabsorption will depend on the underlying cause and any identified deficiencies. For example:

  • Antibiotics: Metronidazole is commonly used.
    • Mechanism of action: It is bactericidal, inhibiting bacterial DNA synthesis and leading to bacterial death.
    • Dosage: Typically 200–400 mg three times a day orally for 7–10 days.
    • Side effects: May include dry mucous membranes and a metallic taste.

Management:

A. Diet:

  • Gluten-free diet for celiac disease.
  • Low-fiber diets.
  • Incorporation of low-fat sources such as medium-chain triglycerides.
  • Avoidance of irritants like spicy foods.

B. Parenteral Fluids and Feeding:

  • Total parenteral nutrition via a central venous line may be necessary for severe cases.

Supplementation:

  • Vitamin B12 injections and oral iron supplements may be required.
  • Enzyme replacement therapy may be prescribed for those lacking intestinal enzymes.
  • Anti-spasmodic medications can help reduce abdominal cramping and diarrhea.

Specific Conditions:

  • Individuals with cystic fibrosis or chronic pancreatitis may need pancreatic supplements.
  • Those with lactose intolerance or non-tropical sprue (gluten enteropathy) should modify their diets to avoid triggering foods.

Once an oral diet is well tolerated, patients are typically prescribed a high-protein, low-fat, high-calorie diet supplemented with additional nutritional supplements. Specific dietary plans, such as a gluten-free diet for individuals with celiac disease, should be implemented as needed. Nurses play a crucial role in educating patients about the significance of adhering to their prescribed diet and ensuring compliance. They should assist patients in understanding the importance of their diet regimen and encourage consistent intake. Additionally, maintaining strict records of fluid intake and food consumption through fluid balance and food intake charts is essential.

Specific nursing management:

When caring for patients with malabsorption syndrome, nurses should employ a problem-solving approach such as the nursing process due to the diverse causes and severity levels of the syndrome. The main areas of assessment include:

  1. Management of Diarrhea and Steatorrhea-Related Problems:
    • Addressing issues like incontinence, perianal excoriation, and fatigue.
  2. Ensuring Adequate Nutritional Intake:
    • Focusing on strategies to ensure patients receive sufficient nourishment despite malabsorption challenges.
  3. Psychological Assessment:
    • Assessing for signs of depression, grief, or anger, which may arise from the loss of normal health,.

In addition to these assessments, nurses should provide comprehensive general care to severely ill patients who require complete bed rest. Special attention should be given to oral hygiene, pressure area care, and promoting deep breathing exercises to maintain overall well-being.

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Peptic ulcers | Nursing Management

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Introduction

A peptic ulcer is characterized by the erosion or breakage of the mucous membrane or tissues within the digestive tract, which are regularly exposed to gastric juices containing hydrochloric acid (HCl) and pepsin. This erosion can extend through the muscle layer and even perforate the outer layers, leading to bleeding or perforation. Essentially, a peptic ulcer involves ulceration that affects the mucosal lining and deeper structures of the upper gastrointestinal tract and is caused by the corrosive action of gastric juices. It manifests as an excavation or hollowed-out area formed within the mucosal wall of the esophagus, stomach, or duodenum.

Epidemiology

  • The highest frequency occurs between the ages of 40 and 60.
  • The peak age for duodenal ulcers is between 30 and 60 years.
  • Gastric ulcers typically peak in individuals aged 50 and older.
  • The male-to-female ratio for duodenal ulcers is 2-3:1.
  • For gastric ulcers, the male-to-female ratio is 1:1.
  • Approximately 80% of peptic ulcer diseases (PUD) manifest as duodenal ulcers, while gastric ulcers account for about 15%

Common Sites:

  • Lower esophagus
  • Stomach
  • Proximal portion of the duodenum

Types

Ulcers can be classified according to their degree and location.

Type according to degree:

  • Peptic ulcers may be acute or chronic. Acute ulcers are often multiple and usually located in the fundus of the stomach. These ulcers are thought to be stress-related, superficial, and self-limiting. Occasionally, they penetrate a blood vessel, causing hemorrhages of varying degrees of severity.
  • Chronic ulcers are more common than acute ulcers. These ulcers usually occur as a single lesion with margins that are thickened, hyperemic, and edematous. Chronic ulcers tend to recur frequently, causing extensive scarring.

Type according to location:

  • Esophageal ulcers: These ulcers affect the lower portion of the esophagus and are usually due to a weaker esophageal sphincter, which allows gastric contents to escape into the esophagus.
  • Gastric ulcers: These occur in the stomach, mainly in the lesser and greater curvatures and pyloric antrum. The occurrence is due to the defective ability of the stomach to heal faster.
  • Duodenal ulcers: These are the commonest and are seen in the first portion of the duodenum. Ulcers result from the high secretion of hydrochloric acid.

Etiology

The erosion of the gastric mucosa is caused by the digestive action of hydrochloric acid and pepsin, although the exact cause is not fully understood. However, several factors precipitate the occurrence of peptic ulcers:

  1. The gram-negative bacteria Helicobacter pylori, present in 70% of patients with gastric ulcers and 95% of patients with duodenal ulcers, has been associated with peptic ulcers.
  2. Emotional factors: Emotional tension, anxiety, frustration, and stress may cause an imbalance in the autonomic nervous system, resulting in increased vagal stimulation of gastric secretion.
  3. Inflammation: Gastritis and trauma to the mucosa reduce the resistance of the membrane to digestion. Cell destruction is accelerated, and cell reproduction, which normally renews the superficial layers quickly, may be retarded.
  4. Hereditary factors: gastric ulcers are common in people with type A blood, while duodenal ulcers are common in people with type O blood. Duodenal ulcers are three times more common in first-degree relatives of duodenal ulcer patients than in the general population.
  5. Trauma and serious illness: Critical illnesses, especially those characterized by hypotension or respiratory insufficiency, may complicate peptic ulcers. Conditions such as severe burns, shock, etc., may lead to peptic ulceration.
  6. Prolonged use of irritants: Certain drugs, including non-steroidal anti-inflammatory drugs (NSAIDs), may predispose to peptic ulcer disease (e.g., acetylsalicylic acid, adrenal steroids, indomethacin, and phenylbutazone). Alcohol inhibits prostaglandin secretion. Nicotine in cigarette smoking inhibits pancreatic secretion of bicarbonate; it also may accelerate the emptying of gastric acid into the duodenum and promote mucosal breakdown.
  7. Bile Reflux: The reflux of bile and pancreatic enzymes into the stomach due to an incompetent pyloric sphincter may lead to a gastric ulcer. The bile salts damage the gastric mucosa, predisposing it to ulceration.
  8. Normal aging may also wear down the pyloric sphincter, which in turn permits the reflux of bile into the stomach.
  9. Zollinger Ellison Syndrome: A condition characterized by excessive production of hydrochloric acid, which erodes the gastric mucosa.

Epidemiology

Duodenal ulcers are very common, occurring 2–3 times more frequently than gastric ulcer disease.

Pathophysiology

Ulceration occurs due to a decrease in the resistance of the gastric mucosa to pepsin and acid injury. After the ingestion of food, acetylcholine, gastrin, and histamine bind to specific receptors and stimulate the parietal cells in the fundus of the stomach to secrete gastric acid. The parietal cells, with the assistance of H+ and K+ ATPases, transport the HCL to the stomach lumen. Meanwhile, the chief cells in the stomach secrete pepsinogen, which converts to pepsin in the presence of HCL to break down food.

Duodenal cells in the epithelium secrete a mucus barrier to protect the lining of the gastric-duodenal area. This mucus barrier dilutes the secretion of acid and provides a protective coating against acid action. Peptic ulcers may develop when the secretory output of hydrochloric acid exceeds that of pepsin, thereby eroding the gastric mucosa membrane due to inadequate defense secretion of mucus to neutralize the imbalance, thereby promoting ulcer development.

Signs and symptoms

Signs and symptoms of peptic ulcers include:

  • Epigastric pain: gnawing or burning pain in the upper abdomen, often related to food intake and radiating to the back due to erosion of the mucosal lining.
  • Heartburn (pyrosis): A burning sensation experienced in some patients due to excessive acid presence in the esophagus and stomach.
  • Vomiting: Occurs due to severe pain and may also be caused by obstruction resulting from muscular spasms of the pylorus.
  • Weight loss is especially common in individuals with gastric ulcers.
  • Dyspepsia: Symptoms include belching, bloating, distention, and intolerance to fatty foods.
  • Chest discomfort
  • Anorexia: loss of appetite.
  • Hematemesis, or melena, results from gastrointestinal bleeding from eroded small blood vessels. Melena stool, characterized by black, tarry stool, is more common in duodenal ulcers.
  • Constipation: Occurs due to inadequate intake of fluids and fiber-rich foods.

Characteristic differences between gastric ulcers and duodenal ulcers:

Location of the Lesion:

  • Gastric ulcers are predominantly found in the antrum of the stomach, as well as in the body and fundus.
  • Duodenal Ulcers: typically occur in the first 2cm of the duodenum.

Lesion Characteristics:

  • Gastric Ulcers: superficial lesions with smooth margins, often round, oval, or cone-shaped.
  • Duodenal Ulcers: Penetrating lesions associated with deformity of the duodenum from the healing of previous ulcers.

Gastric Secretion:

  • Gastric Ulcers: normal to decreased secretion.
  • Duodenal Ulcers: increased secretion.

Incidence and Peak Age:

  • Gastric Ulcers: Higher incidence in women; peak age typically between 50 and 60 years; more common in people of lower socioeconomic status.
  • Duodenal Ulcers: higher incidence in men but also prevalent in post-menopausal women; peak age typically between 35 and 45 years.

Associated Factors:

  • Gastric Ulcers: are associated with an incompetent pyloric sphincter and bile reflux.
  • Duodenal Ulcers: are associated with other diseases such as pancreatic disease and Zollinger-Ellison syndrome.

Clinical Manifestations:

  • Gastric Ulcers: Burning or gaseous pressure in the high left epigastric region, pain occurs 1-2 hours after meals and is aggravated by food, weight loss, and hematemesis may occur.
  • Duodenal Ulcers: Burning and crampy pain across the mid-epigastrium and upper abdomen, pain occurs 2-4 hours after meals but is relieved with food, weight may be normal or the patient may gain more weight, melena may occur.

Blood Group:

  • No significant difference was observed.
  • Duodenal Ulcers: common in blood group O.

Cancerous Tendencies:

  • Gastric Ulcers: More common to develop cancer.
  • Duodenal Ulcers: Less common to develop cancer.

Diagnosis:

History Taking:

  • Assess abdominal pain, including location, timing, severity, associated symptoms, and precipitating factors.

Physical Assessment:

  • Carefully examine and palpate the abdomen, focusing on pain, typically present in the upper epigastrium, left of the midline.

Endoscopy (Esophagogastroduodenoscopy):

  • Visualize and identify inflammatory changes, ulcers, and lesions in the upper gastrointestinal tract, including the duodenal mucosa.

Special Radiology:

  • Perform a barium swallow and barium meal to visualize the ulcer after the patient has ingested barium sulfate.

Stool Examination:

  • Detect the presence of blood (occult or fresh) in the stool, which may indicate bleeding from the gastrointestinal tract.

Biopsy:

  • Conduct a biopsy for gastric ulcers to determine the benign or malignant status of the lesion.

Gastric Analysis:

  • Aid in differentiating gastric ulcers from gastric cancer by analyzing gastric secretions.

Exfoliative Cytology:

  • Examine secretions and cells brushed or scraped from the mucous membranes to further aid in diagnosis.

Drug Therapy Objectives:

  1. Provide pain relief.
  2. Eradicate the H. pylori infection.
  3. Promote ulcer healing by reducing gastric secretions and protecting the mucosa from further damage.
  4. Prevent the recurrence of ulcers.

Eradication Therapy

First-Line Therapy:

A recommended regimen for eradicating Helicobacter pylori in patients with gastric and duodenal ulcers is the use of a proton pump inhibitor (PPI) in combination with two antibiotics, such as Omeprazole, clarithromycin, and metronidazole.

Omeprazole:

  • Dosage: 20mg orally twice daily for 4 to 8 weeks.
  • Action: It inhibits the activity of the acid pump and binds to hydrogen-potassium adenosine triphosphatase to block the formation of gastric acid.
  • Side Effects: headache, hallucinations, dizziness, diarrhea, abdominal pain, nausea, vomiting, constipation.
  • Nursing Implications: Caution the patient not to perform hazardous activities if dizziness occurs; instruct the patient to swallow capsules whole and not to open or crush them.

Amoxicillin:

  • Dosage: 500mg three times daily orally.
  • Action: Blocks protein synthesis.
  • Side Effects: Nausea, vomiting, diarrhea, abdominal pain, or discomfort.
  • Nursing Implications: Use cautiously in patients with hepatic or renal impairment; obtain a urine specimen for culture and sensitivity tests before the first dose. Begin therapy pending results; monitor the patient for superinfection.

Metronidazole:

  • Dosage: 400–500 mg orally three times daily.
  • Side Effects: metallic taste, nausea, and vomiting.
  • Nursing Implications: Instruct the patient to take the drug with food to minimize gastrointestinal discomfort.

Second-Line Therapy:

In cases where first-line therapy fails, a second-line regimen may be considered. This regimen typically includes a proton pump inhibitor along with bismuth, metronidazole, and tetracycline.

Bismuth:

  • Dosage: 120mg four times daily.
  • Action: Provides a protective coating to the gastrointestinal tract.
  • Side Effects: May cause darkening of the tongue and stools.
  • Nursing Implications: Monitor for signs of gastrointestinal upset and dark stools.

Metronidazole:

  • Dosage: 400mg twice daily.
  • Side Effects: metallic taste, nausea, and vomiting.
  • Nursing Implications: Administer food to reduce gastrointestinal side effects.

Tetracycline:

  • Dosage: 500mg twice daily.
  • Action: inhibits bacterial protein synthesis.
  • Side Effects: photosensitivity, gastrointestinal upset, tooth discoloration (avoid use in children).
  • Nursing Implications: Advise patients to avoid prolonged exposure to sunlight and use sun protection measures. Monitor for gastrointestinal side effects and tooth discoloration.

Other Drugs

  1. Antacids:
    • Mechanism: Antacids work by neutralizing gastric acid, thereby decreasing acidity in the stomach. They do not influence ulcer healing or prevent recurrence. Antacids aim to raise the pH in the stomach to around 3.0–3.5. They are typically taken after meals.
    • Examples: aluminum hydroxide, magnesium trisilicate.
  2. Histamine Receptor Antagonists:
    • Mechanism: Histamine receptor antagonists block the action of histamine, which stimulates acid secretion in the stomach. They are effective in managing ulcer disease by inhibiting acid secretion. Examples include Ranitidine (150mg twice daily) or Cimetidine (400mg twice daily for 4-6 weeks).
  3. Mucosal Barrier Fortifiers:
    • Mechanism: Mucosal barrier fortifiers, such as sucralfate, stimulate mucus production and enhance ulcer healing. They form a protective barrier by adhering to the ulcer surface, preventing further damage to the mucosa. Sucralfate is typically administered as 1g orally four times daily or 2g twice daily, 1 hour before meals and at bedtime. It should not be administered within 30 minutes of antacids or other drugs.
  4. Anticholinergic Drugs:
    • Mechanism: Anticholinergic drugs, like propantheline, are less commonly used compared to histamine receptor antagonists. They reduce gastric motility and secretion by decreasing vagal stimulation. This delay in gastric emptying time may promote ulcer healing and provide pain relief. However, they are not used in cases of bleeding or pyloric obstruction.

Nursing Management

Aims

  • Alleviating Symptoms and Promoting Healing
  • Reducing Anxiety
  • Maintaining Nutritional Requirements
  • Providing Education about Disease and Management
  • Preventing Complications

Hospitalization Considerations:

  • Hospitalization may not always be necessary
  • If adherence to treatment is challenging or home environment is not conducive, hospitalization may be required
  • The duration of hospitalization depends on symptom relief and patient understanding of treatment plan

Creating a Supportive Environment

  • Promoting Rest: Ensure the environment supports both mental and physical rest. Nurse the patient in a quiet setting to minimize disturbances and promote relaxation, especially since patients with peptic ulcers experience severe pain.
  • Ventilation: Ensure the environment is well-ventilated to enhance comfort and prevent feelings of stuffiness or discomfort.
  • Stress Reduction: Remove stressful stimuli from the environment as much as possible. Stress can increase vagal activity, exacerbating the symptoms of peptic ulcers. Creating a calm and peaceful environment can help alleviate stress and promote healing.
  • Comfort: Provide amenities that contribute to the patient’s comfort, such as adjusting the room temperature to a comfortable level, providing soft bedding, and ensuring adequate lighting.
  • Safety: Ensure the environment is safe and free from hazards that could potentially harm the patient. Keep walkways clear, and ensure that any equipment or furniture is properly secured to prevent accidents.
  • Privacy: Respect the patient’s privacy by maintaining confidentiality and providing them with a sense of personal space. This can contribute to their overall sense of well-being and comfort during their stay.

Rest

Rest, both mental and physical, plays a crucial role in reducing gastric activity and promoting healing in individuals with peptic ulcers. While a brief period of bed rest is essential, patients may also be encouraged to remain ambulatory with some restrictions on activity and an increase in rest hours. In severe cases, it may be necessary for patients to take time away from work, although for some, the anxiety caused by financial strain or disruption to their routine may outweigh the benefits of rest.

Creating a quiet and pleasant environment is paramount, as is ensuring physical comfort and providing undisturbed rest periods. Visitors who may evoke unpleasant feelings should be avoided, and diversion therapy can help alleviate anxiety. Nurses should listen attentively to patients, encouraging them to develop coping mechanisms for stressful situations that exacerbate symptoms. Providing perspective and offering constructive suggestions can help patients manage their anxiety levels.

In some cases, a sedative or tranquilizer may be prescribed to promote relaxation. It’s important to discourage visitors who may agitate the patient until their condition improves, allowing them the peace and tranquility necessary for healing.

Pain Relief

Assessment of the patient’s pain is essential, involving both verbal communication and observation of non-verbal cues such as grimacing or rubbing the affected area. Administer prescribed medications like Panadol to alleviate pain and enhance comfort, along with other medications aimed at promoting ulcer healing. Additionally, advise the patient to avoid highly spiced foods, as they can exacerbate pain and hinder the healing process. Providing diversional therapy, such as reading books or watching TV, can also help distract the patient from pain and promote relaxation.

Psychological Care

Effective psychological care plays a crucial role in the treatment of peptic ulcers, particularly due to their potential association with emotional factors. Begin by explaining the condition to the patient and their significant others in simple terms, covering aspects such as the disease process, affected parts of the body, associated signs and symptoms, causes, treatment options, and potential complications. This comprehensive explanation serves to impart knowledge and alleviate anxiety.

Encourage the significant others to refrain from alarming the patient with negative news or involving them in serious decision-making processes, as this could exacerbate stress. Instead, create an environment where the patient feels comfortable expressing their fears and concerns openly. Furthermore, involve the patient in developing plans for their care, fostering a sense of cooperation and empowerment in their treatment journey.

Observations

Continuous monitoring of the patient’s general condition is essential to gauging improvement or deterioration. Establish baseline data for vital signs, including pulse and blood pressure, which may indicate hemorrhage, as well as temperature and respirations, which can be affected by severe peptic ulcers.

Observe the patient for pain, noting its location and any exacerbating factors, such as specific foods. Monitor for vomiting episodes and examine the contents of the vomitus, as well as observe stool characteristics. Document and promptly report all findings to the responsible nurse.

Track the patient’s response to treatment and remain vigilant for any potential side effects of prescribed medications. Additionally, monitor for complications such as hemorrhage, which may manifest as dizziness, low blood pressure, a rapid, feeble pulse, or pyloric obstruction, indicated by vomiting of undigested food. Observe the patient’s dietary habits and assist in identifying foods that either alleviate or exacerbate pain, contributing to personalized care and symptom management.

Nutrition and Fluid Management

Nutrition plays a crucial role in the treatment of patients with peptic ulcers, as certain foods can either exacerbate or alleviate symptoms. Identify and avoid foods known to cause pain, as well as those that are highly seasoned or known to produce gas, as they can worsen the patient’s condition. Instead, provide a well-balanced diet rich in proteins to support ulcer healing and roughage to prevent constipation, a common issue.

Offer food in small, frequent portions to promote appetite and reduce the likelihood of vomiting. Encourage fluid intake, either orally or intravenously, depending on the patient’s condition, to prevent dehydration resulting from vomiting and to help neutralize hydrochloric acid in the stomach. This approach supports overall patient comfort and aids in symptom management.

Elimination Management

Monitor intake and output closely, recording measurements to prevent fluid overload. Offer a diet rich in roughage to facilitate bowel movements and prevent constipation, a common concern in patients with peptic ulcers. Regularly inspect stool and vomitus for signs of blood, and promptly inform the physician if any abnormalities are noted. Additionally, provide an emesis bowl to assist with vomiting episodes, ensuring patient comfort and cleanliness. These measures contribute to effective elimination management and overall patient well-being.

Exercises and Hygiene Management

Exercises: Initially, patients with peptic ulcers should be placed on total bed rest to prevent stress and excessive stimulation of the vagus nerve, which can increase hydrochloric acid production. As the patient’s condition improves, introduce gentle exercises gradually to prevent complications such as deep vein thrombosis associated with prolonged bed rest.

Hygiene: Provide assistance to patients with bathing to enhance comfort, promote blood circulation, and maintain cleanliness, thereby reducing the risk of infection. Perform oral care regularly to stimulate appetite, prevent halitosis (bad breath), and maintain oral hygiene. Ensure the timely changing of bed linens as needed to maintain cleanliness and prevent skin irritation. These measures contribute to overall patient comfort and well-being while minimizing the risk of complications associated with immobility and poor hygiene.

Patient Education

  • Educate the patient about avoiding precipitating factors such as caffeinated drinks and alcohol ingestion, which can exacerbate symptoms.
  • Assess the patient’s current knowledge of managing the condition to establish a baseline for further education.
  • Determine the patient’s willingness and ability to learn, ensuring comprehension of the condition and its management.
  • Assist the patient in identifying stressors and making modifications to daily routines to reduce stress-induced hypersecretion of gastric acid and pepsin.
  • Discuss dietary plans and provide guidance on implementation both at home and in the workplace.
  • Teach the patient to recognize warning signs and symptoms of recurrent ulcers or complications, and stress the importance of seeking early treatment.
  • Explain the harmful effects of smoking, which directly irritates the gastric mucosa and can worsen symptoms.
  • Provide a rationale for eliminating alcohol, spicy foods, coffee, tea, and cola from the diet, emphasizing their impact on ulcer symptoms.
  • Offer written materials on the condition to reinforce understanding and provide additional resources for reference.
  • Emphasize the importance of adhering to prescribed medication regimens and educate on the potential side effects of the drugs. Discourage the use of unprescribed drugs such as aspirin.
  • Reinforce the need for regular follow-up appointments to monitor progress and adjust treatment as needed.

Complications

Hemorrhage: This is the most common complication associated with peptic ulcer disease, occurring when the ulcer erodes a blood vessel. Signs of hemorrhage include vomiting blood (hematemesis) and passing black, tarry stools (melena). In cases of massive bleeding, patients may experience weakness, apprehension, dizziness, and faintness, which can progress rapidly to prostration and loss of consciousness. Physical signs include pale, cold, and clammy skin, a rapid and thready pulse, and abnormally low blood pressure. Rapid respirations may indicate air hunger and hypoxemia. If a large blood vessel is eroded, signs and symptoms appear more rapidly, and collapse can occur quickly.

Perforation: Perforation is a serious and potentially life-threatening complication resulting from the progressive erosion of ulcers through the layers of the gastrointestinal wall, including the submucosal, muscular, and serous layers. When the serous membrane is breached, stomach or duodenal contents can leak into the peritoneal cavity, leading to generalized peritonitis due to chemical irritation and infection. Perforation is more common in duodenal ulcers and can occur even in individuals with no previous ulcer history.

Symptoms of perforation include sudden and severe abdominal pain starting in the mid-epigastric region and spreading throughout the abdomen. The patient may exhibit pallor, cold clammy skin, a rapid pulse, shallow, grunting respirations, and may experience nausea and vomiting. Upon examination, the abdomen becomes tender, rigid, and board-like. Patients may adopt a knee-chest position to alleviate tension on the abdominal muscles. Perforation can lead to complications such as bacterial septicemia, hypovolemic shock, and paralytic ileus, further complicating the patient’s condition and requiring prompt medical attention.

Peritonitis -can develop as a consequence of perforation into the peritoneal cavity. Gastric outlet obstruction occurs due to edema, inflammation, and fibrous scar formation. Symptoms include abdominal bloating, nausea, and vomiting. Persistent vomiting can lead to alkalosis due to the loss of acid gastric juice in vomit, resulting in hypokalemia from the loss of chloride ions.

Malignancy -may arise from the chronic ulceration-induced regeneration of epithelium. Penetration occurs when an ulcer on the posterior wall of the duodenum or stomach perforates into adjacent structures such as the pancreas, liver, or biliary tree. Patients may experience intensified and constant pain, possibly radiating to the back, which does not respond to antacids or food.

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Gastritis | Nursing Management

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Introduction

Effective management of patients with stomach and duodenal disorders involves a comprehensive approach aimed at alleviating symptoms, promoting healing, and preventing complications. Below are key aspects of management:

Gastritis

Gastritis refers to inflammation of the lining of the stomach. It can be acute, occurring suddenly and lasting for a short period, or chronic, developing gradually and persisting over time.

Pathophysiology of Gastritis

The gastric mucosa is normally shielded from the corrosive effects of stomach acid by prostaglandins. However, when there is damage to the protective barrier, injury occurs. This injury is exacerbated by the release of histamine and stimulation of the vagal nerve, which allows hydrochloric acid to penetrate back into the mucosa. This acid influx damages small blood vessels, leading to swelling, bleeding, and erosion of the stomach lining.

As gastritis progresses, the walls and lining of the stomach become thinner and may atrophy, reducing the function of parietal cells. This decline in parietal cell function results in a loss of intrinsic factor, essential for the absorption of vitamin B12. Consequently, the absorption of vitamin B12 is impaired, leading to pernicious anemia.

Acute Gastritis

Acute gastritis refers to the acute inflammation of the gastric mucosa or submucosa, characterized by the destruction of superficial epithelial cells. The condition typically lasts for a few hours to a few days (Bloom, 2005).

Causes:

  • Thermal Causes: Consumption of very hot fluids or food can lead to thermal injury to the gastric mucosa.
  • Chemical Causes:
    • Ingestion of corrosive substances.
    • Consumption of irritating foods such as spicy foods and alcohol.
    • Certain drugs, including aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs) in large doses, cytotoxic agents, caffeine, corticosteroids, antimetabolites, phenylbutazone, and indomethacin, can cause mucosal erosion.
  • Bacterial Causes: Endotoxins released from infecting bacteria such as Staphylococci, Escherichia coli, Salmonella, and Helicobacter pylori.
  • Conditions: Uremia, shock, prolonged emotional tension, major burns, hepatic diseases, renal diseases, peptic ulcers, and major surgery can precipitate acute gastritis.
  • Bile Reflux: Backflow of bile into the stomach from the bile tract, which connects to the liver and gallbladder, can irritate the gastric mucosa.
  • Exposure to Procedures: Certain medical procedures such as nasogastric tube insertion and endoscopy can irritate the gastric mucosa.

Signs and Symptoms of Acute Gastritis:

  • Sudden Onset: Symptoms typically appear suddenly.
  • Anorexia: Loss of appetite may occur.
  • Nausea and Vomiting: Patients may experience feelings of nausea and episodes of vomiting.
  • Dyspepsia: discomfort or pain in the upper abdomen, often described as indigestion or an upset stomach.
  • Epigastric Pains: Patients may experience varying degrees of pain or discomfort in the epigastric region (upper abdomen).
  • Gastrointestinal Bleeding: Hematemesis (vomiting of blood) and melena (dark, tarry stools) may occur if gastric bleeding occurs.
  • Water Brash Syndrome: Clear fluid may be present in the mouth due to reflex salivation in response to duodenal ulceration.
  • Signs and Symptoms of Pernicious Anemia: Due to the loss of intrinsic factor, patients may exhibit symptoms associated with pernicious anemia, such as fatigue, weakness, and pallor.
  • Colic Diarrhea: Following intake of contaminated food, patients may experience colicky diarrhea 2-4 hours later if gastritis is due to food poisoning.
  • Fever: Fever may be present in some cases, especially if the gastritis is caused by an infectious agent.

Diagnosis of Acute Gastritis:

  • Endoscopy/Gastroscopy: Visual examination of the stomach using an endoscope will reveal inflamed gastric membranes.
  • Laboratory Tests:
    • Full Blood Count (FBC): Low hemoglobin levels may be detected due to concealed bleeding, indicated by the presence of occult blood in vomitus and stool. Elevated erythrocyte sedimentation rate (ESR) may also be observed, indicating inflammation.
  • Histological Examination: Biopsy specimens obtained during endoscopy can be examined histologically to assess the severity and nature of inflammation.
  • Serologic Testing: Serological tests for antibodies against Helicobacter pylori or a breath test may be performed to detect the presence of H. pylori infection, a common cause of gastritis.
  • Gastric Acid Analysis: Measurement of gastric acid levels can reveal increased hydrochloric acid (HCl) secretion, which may contribute to the development of gastritis.

Medical and Nursing Management:

The gastric mucosa possesses the ability to repair itself following a mild attack of gastritis. Typically, patients recover within a day, although a diminished appetite may persist for an additional 2 or 3 days. Management primarily focuses on symptom relief and supportive care.

  • Fluid and Food Management:
    • During episodes of vomiting, oral fluids and food should be withheld to prevent further irritation to the stomach.
    • Once vomiting subsides, oral fluids and non-irritating foods can be gradually reintroduced based on the patient’s tolerance.
    • The diet can then progress to a normal intake as tolerated by the patient.
  • Intravenous Fluids:
    • If gastritis persists beyond 12–18 hours or if dehydration and electrolyte imbalance are evident, intravenous fluids are administered.
    • Hospitalization may be necessary in such cases, and complete bed rest is recommended to facilitate recovery.

The following medications may be prescribed:

  • Antiemetics: Promethazine can be prescribed to alleviate symptoms of nausea and vomiting. However, it should be avoided if the cause of gastritis is due to corrosive substances.
  • Anticholinergics: Atropine may be administered to decrease gastric secretions and induce relaxation of smooth muscle.
  • Cimetidine: This medication is typically given to reduce gastric acid secretion, especially in cases where there is associated hemorrhage with gastritis.

In cases where gastritis is caused by the ingestion of strong acids or alkalis, emergency treatment involves diluting and neutralizing the offending agent. To neutralize acids, common antacids, such as aluminum hydroxide, are used. For neutralizing an alkali, diluted lemon juice or diluted vinegar can be employed.

Chronic gastritis

Chronic gastritis is a long-term degeneration of the mucous membranes of the stomach, often resulting from prolonged dietary indiscretion or alcohol abuse.

Causes

  • Helicobacter pylori infection (most common cause).
  • Alcohol abuse.
  • Thyroid disease.
  • Diabetes mellitus.
  • Radiation therapy.
  • Repeated episodes of acute gastritis.
  • Autoimmune conditions such as pernicious anemia.
  • Smoking.

Signs and symptoms:

  • Loss of appetite leads to weight loss.
  • Nausea and vomiting (hematemesis), which may provide temporary relief from pain due to irritation of the gastric mucosa.
  • Dyspepsia (indigestion) results from impaired gastric function.
  • Flatulence (excessive gas) due to impaired gastric function.
  • Epigastric pain (heartburn) is caused by the regurgitation of gastric contents.
  • Abdominal pain is due to erosion of the gastric mucosa.
  • Passage of dark, tarry stools (melena) resulting from gastric bleeding.
  • Constipation is followed by diarrhea due to enteritis.
  • Slow progression of symptoms.

Diagnosis:

  • Patient history indicating recurrent episodes of acute gastritis.
  • Barium meal, revealing inflammation of the gastric mucosa.
  • Endoscopy or gastroscopy showing inflammation of the gastric mucosa.
  • Stool testing for occult blood.
  • Complete blood count (CBC) revealing low hemoglobin levels due to bleeding.
  • Gastric acid analysis indicates increased hydrochloric acid (HCl) secretion.

Treatment:

  • Chronic gastritis is managed through dietary modifications, rest promotion, stress reduction, and pharmacotherapy.
  • Encourage the patient to chew food thoroughly before swallowing.
  • Helicobacter pylori infection may be treated with a combination of drugs such as amoxicillin, metronidazole (Flagyl), and omeprazole (triple therapy).
  • Administer antiemetic drugs to alleviate nausea and vomiting, for example, promethazine 25–50 mg either intramuscularly or intravenously for 3 days, or metoclopramide (Plasil) 10–20 mg three times daily for 3 days.
  • Antacids can be given to alleviate pain or discomfort, such as aluminum hydroxide 200–400 mg three times daily for 7 days.
  • Histamine receptor blockers help reduce the production of hydrochloric acid; for instance, cimetidine 200–400 mg three times daily for 14 days.

Nursing Care for Gastritis

Aims

  • Prevent complications.
  • Alleviate signs and symptoms.
  • Assist in the healing process.
  • Reduce anxiety.

Environment

The patient is cared for in a general medical ward where cleanliness and proper ventilation are maintained to promote adequate air circulation and create a calm environment conducive to rest and recovery.

Positioning

The patient is positioned in a comfortable manner, preferably in a semi-fowler’s position, to prevent the regurgitation of gastric juices and to enhance respiratory function. The semi-fowler’s position involves reclining the patient’s upper body at an angle of approximately 30 to 45 degrees, which helps reduce pressure on the abdomen and minimizes reflux while facilitating ease of breathing.

Rest

Ensure a noise-free environment to promote rest and uninterrupted sleep for the patient. Perform nursing activities collectively to minimize disturbances and encourage restful periods. This includes coordinating tasks such as medication administration, assessments, and procedures to avoid unnecessary interruptions to the patient’s rest.

Observations

Regularly assess the patient’s general condition to determine if there are improvements, stability, or worsening of symptoms. Monitor vital signs including temperature, pulse rate, respiratory rate, and blood pressure, and document the findings. Elevated temperature may indicate the presence of infection, while a rapid pulse and low blood pressure could indicate bleeding.

Examine stool and vomitus for characteristics such as color, consistency, volume, and odor. If blood is present in stool or vomitus, provide ice drinks to the patient to help constrict blood vessels and minimize bleeding. Check for abdominal tenderness and observe for any signs of complications such as gastric ulcers.

Patient Weight Monitoring

Perform daily weighing of the patient to monitor for changes in weight, which can indicate fluid retention or loss. This helps in assessing the patient’s hydration status and response to treatment. Document weight measurements accurately to track trends over time.

Psychological Care

It is essential to communicate effectively with the patient and their relatives to alleviate anxiety and foster cooperation. Explain the condition in simple terms, including possible causes, the disease process, treatment options, and reasons for certain restrictions. Encourage the patient to ask questions and provide accurate answers to help them understand their condition better. Involving both the patient and their relatives in the care plan promotes independence and reduces dependency.

Nutrition and Fluids

Provide balanced, nutritious meals containing proteins, vitamins, and carbohydrates to support healing and boost immunity. Serve food in small, frequent amounts to promote appetite and prevent vomiting, especially if the patient experiences anorexia. Avoid spicy foods as they may exacerbate the condition. Ensure adequate fluid intake, either orally or intravenously, to prevent dehydration and flush out toxins. Discourage alcohol consumption as it can worsen the condition and interfere with the healing process.

Elimination

Monitor the patient’s intake and output, including observing stool and vomitus for consistency, color, amount, and odor. Record and report any abnormalities. Additionally, observe the patient’s bowel patterns to identify any changes or irregularities. Encourage the patient to consume foods rich in roughage and increase fluid intake to prevent constipation.

Exercises

Initially, the patient may require total bed rest, but as their condition improves, encourage them to engage in passive exercises. These exercises help prevent complications such as deep vein thrombosis and promote blood circulation. Passive exercises involve gentle movements of the limbs performed by the caregiver while the patient remains in a relaxed position. These exercises can help maintain muscle tone and prevent stiffness during periods of immobility.

Hygiene

If the patient is unable to bathe independently, provide a bed bath to ensure hygiene, comfort, and promote blood circulation. Perform oral care to prevent mouth infections and stimulate appetite. Additionally, provide nail care to prevent the accumulation of dirt. Change bed linens promptly when soiled or dirty to maintain cleanliness and prevent skin irritation.

IEC (Information, Education, Communication)

  1. Explain to the patient the importance of rest in aiding recovery and managing symptoms.
  2. Educate the patient about the disease process, including its causes, symptoms, and potential complications.
  3. Advise the patient to avoid spicy foods and the dangers of consuming unprescribed drugs, which can exacerbate symptoms.
  4. Help the patient identify factors that may worsen their symptoms, such as stress or certain dietary choices.
  5. Stress the importance of medication compliance to ensure effective treatment and symptom management.
  6. Emphasize the significance of attending scheduled review appointments with healthcare providers.
  7. Teach the patient to recognize signs and symptoms of potential complications and when to seek medical attention.
  8. Discuss the necessity of making lifestyle changes, such as abstaining from alcohol consumption, to improve overall health and manage the condition effectively.

Complications

Complications of gastritis can vary in severity and may include:

  1. Gastric ulcers: Prolonged inflammation of the gastric mucosa can lead to the formation of ulcers in the stomach lining, which may cause pain, discomfort, and bleeding.
  2. Haemorrhage: Severe inflammation and erosion of the stomach lining can result in significant bleeding, leading to haemorrhage. This can manifest as vomiting of blood (haematemesis) or passing of black, tarry stools (melena).
  3. Anaemia: Chronic bleeding from gastric ulcers or erosion of blood vessels in the stomach can lead to iron deficiency anaemia due to the loss of red blood cells and decreased iron stores.
  4. Obstruction: Inflammation and scarring of the stomach lining may cause narrowing of the stomach’s passageway, leading to obstruction of food flow. This can result in symptoms such as nausea, vomiting, and abdominal pain.
  5. Perforation: Severe inflammation and erosion of the stomach wall can lead to the formation of a hole or perforation, allowing gastric contents to leak into the abdominal cavity. This is a medical emergency and requires immediate intervention to prevent peritonitis.
  6. Peritonitis: Perforation of the stomach wall can lead to contamination of the peritoneal cavity with gastric contents, resulting in peritonitis—an inflammation of the peritoneum. Peritonitis is a life-threatening condition that requires prompt medical attention and treatment with antibiotics.
  7. Stomach cancer: Chronic gastritis, especially when caused by infection with Helicobacter pylori or long-term exposure to irritants such as alcohol or tobacco, can increase the risk of developing stomach (gastric) cancer over time. Regular monitoring and appropriate management of gastritis are essential for reducing this risk.

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Oral and esophageal disorders | Nursing Management

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Introduction

Oral and esophageal disorders refer to a range of medical conditions that affect the mouth (oral cavity) and the esophagus (the tube connecting the throat to the stomach). These disorders can encompass various conditions such as infections, inflammation, structural abnormalities, tumors, and functional disorders affecting the normal functioning of these areas.

Oral disorders

1. Stomatitis

Stomatitis is defined as inflammation of the mucosa inside the mouth. It can arise from various oral conditions or may be associated with other diseases.

Types of stomatitis:

  1. Simple Catarrhal Stomatitis: Simple catarrhal stomatitis involves inflammation of the mucous membranes within the mouth, accompanied by an increased flow of mucus and exudates. This type of stomatitis is more commonly observed in children compared to adults.

Causes:

  1. Microorganisms such as bacteria can contribute to the development of stomatitis, leading to inflammation of the mouth mucosa.
  2. Poor oral hygiene or neglect of oral care can create an environment conducive to stomatitis.
  3. Consumption of hot foods or drinks may irritate the mouth lining, exacerbating stomatitis symptoms.
  4. Wounds caused by foreign bodies in the mouth can introduce infection and inflammation, triggering stomatitis.
  5. Exposure to strong acids or alkalis can lead to corrosion of the oral tissues, potentially causing stomatitis.
  6. Systemic infections, such as viral or fungal infections, can manifest as stomatitis.

Signs and symptoms:

  1. A low-grade fever may accompany stomatitis as the body responds to inflammation.
  2. Dry mucous membranes in the mouth can cause discomfort and contribute to the development of sores.
  3. The presence of sores or ulcers in the mouth is a common symptom of stomatitis.
  4. Pain in the mouth, especially while eating or drinking, is a characteristic symptom of stomatitis.
  5. Redness of the mucous membranes may indicate inflammation associated with stomatitis.
  6. Loss of appetite and a preference for cold drinks may occur due to discomfort associated with stomatitis.

Treatment:

  1. Administration of antipyretics such as paracetamol, taken at a dose of 1 gram three times a day, can help alleviate the fever and discomfort associated with stomatitis.
  2. Mouthwashes containing antiseptic agents can help reduce the microbial load and promote the healing of oral lesions.
  3. Consumption of a soft diet can minimize irritation to the mouth and facilitate the healing of ulcers.
  4. Treatment of any underlying systemic conditions contributing to stomatitis is essential for comprehensive management of the condition.

2. Vincent’s Stomatitis

Vincent’s stomatitis, also known as acute necrotizing ulcerative gingivitis (ANUG), is a severe inflammation of the mouth and gums primarily caused by bacterial infection, often associated with poor oral hygiene and immunosuppression.

Causes:

  1. Bacterial infection: Vincent’s stomatitis is primarily caused by bacterial overgrowth, particularly species such as Fusobacterium and Prevotella.
  2. Poor oral hygiene: Inadequate dental care and hygiene practices can create an environment conducive to bacterial proliferation and subsequent stomatitis.
  3. Immunosuppression: Weakened immune system function, whether due to underlying medical conditions or medications, can increase susceptibility to bacterial infections and exacerbate the severity of stomatitis.

Signs and symptoms:

  1. Pain in the mouth: Patients with Vincent’s stomatitis often experience significant discomfort and pain, particularly in the affected areas of the mouth and gums.
  2. Swelling of the affected parts: Inflammation and swelling of the gums and surrounding tissues are common manifestations of Vincent’s stomatitis.
  3. Bleeding from the gums: Gingival bleeding, especially during brushing or eating, may occur due to tissue inflammation and breakdown.
  4. Redness of the mucous membrane: The oral mucosa may appear red and inflamed, indicative of the underlying inflammatory process.
  5. Bad taste: Patients may report a foul or unpleasant taste in the mouth, often due to bacterial overgrowth and tissue breakdown.
  6. Halitosis: Persistent bad breath may result from bacterial infection and tissue necrosis characteristic of Vincent’s stomatitis.
  7. Fever due to infection: Systemic symptoms such as fever may accompany severe cases of Vincent’s stomatitis, reflecting the body’s immune response to bacterial invasion.

Diagnosis:

  • Physical examination: Clinical evaluation may reveal characteristic features such as mouth and gum swelling, inflamed and red gums, and ulceration.
  • Dental x-rays: Radiographic imaging may be used to assess the extent of dental and periodontal involvement.
  • History-taking: Gathering information about the patient’s dental and medical history can aid in diagnosis and treatment planning.

Treatment:

  • Oral antibiotics: Antibiotics such as penicillin or erythromycin are commonly prescribed to combat bacterial infection and reduce inflammation.
  • Antiseptic mouthwash: Antimicrobial mouth rinses containing chlorhexidine or hydrogen peroxide can help control bacterial growth and promote oral hygiene.
  • Hydrogen peroxide rinses: Rinsing with a diluted hydrogen peroxide solution can aid in cleaning and disinfecting oral wounds and ulcers.
  • Regular brushing: Maintaining good oral hygiene through regular brushing and flossing is essential for preventing bacterial buildup and promoting healing.
  • Professional dental cleaning: Professional dental cleanings may be necessary to remove plaque, tartar, and debris contributing to bacterial proliferation and inflammation.

3. Moniliasis

Oral thrush, also known as moniliasis or candidiasis, is a mouth infection caused by a yeast-like fungus called Candida albicans.

Predisposing Factors: Oral thrush commonly occurs in individuals with:

  • Lowered immunity: Conditions such as HIV/AIDS, diabetes, or undergoing chemotherapy or immunosuppressive therapy can weaken the immune system, making individuals more susceptible to fungal infections.
  • Prolonged use of antibiotics: Antibiotics, particularly broad-spectrum ones like tetracycline and chloramphenicol, can disrupt the normal flora of the mouth, which usually keeps fungal overgrowth in check. This disruption creates an environment conducive to Candida albicans proliferation.

Signs and symptoms:

  • Lesions on the mucous membrane and gums: Oral thrush manifests as white, creamy patches or plaques on the tongue, inner cheeks, roof of the mouth, and gums. These lesions may be painful and bleed easily when disturbed.
  • Discomfort and pain: Patients may experience discomfort or pain while eating or swallowing, especially if the lesions are located in sensitive areas of the mouth.
  • Soreness or burning sensation: The affected areas may feel sore or have a burning sensation, particularly during eating or drinking acidic or spicy foods.

Treatment:

  • Hydrogen peroxide and normal saline mouthwashes: Rinsing the mouth with a solution of hydrogen peroxide or normal saline can help reduce the fungal load and promote the healing of oral lesions.
  • Antifungal medications:
    • Clotrimazole tablets dissolved in the mouth: Clotrimazole is an antifungal medication available in tablet form which can be dissolved in the mouth and used several times a day to combat oral thrush.
    • Nystatin suspension, pastilles or amphotericin lozenges: These antifungal agents are commonly prescribed to treat oral thrush. They work by directly targeting and killing Candida albicans.
    • Fluconazole for oropharyngeal candidiasis: In severe cases or when other treatments fail, oral fluconazole, a systemic antifungal medication, may be prescribed to eliminate the fungal infection.
  • Oral hygiene: Maintaining good oral hygiene practices, such as regular brushing and flossing, can help prevent the recurrence of oral thrush. Additionally, using a soft-bristled toothbrush and avoiding irritating or abrasive mouthwashes can prevent further irritation of oral lesions.

4. Hepatic stomatitis

Hepatic stomatitis, also known as herpetic stomatitis, is a contagious viral infection of the mouth characterized by the development of ulcers and inflammation. It is commonly observed in children.

Causes:

  • Herpes virus hominis: Hepatic stomatitis is often caused by infection with herpes simplex virus type 1 (HSV-1), which is highly contagious and can be transmitted through close contact with an infected individual or by sharing utensils, towels, or personal items.
  • Epstein-Barr virus (EBV): In some cases, Epstein-Barr virus, the causative agent of infectious mononucleosis, may also contribute to the development of hepatic stomatitis.
  • Varicella zoster virus: This virus, which causes chickenpox and shingles, has also been implicated as a potential cause of stomatitis, particularly in individuals with compromised immune systems.

Signs and symptoms:

  • Blisters in the mouth: The initial presentation of hepatic stomatitis often involves the development of fluid-filled blisters or vesicles on the mucous membranes of the mouth, commonly on the tongue or inner cheeks.
  • Decrease in food intake: Patients may experience a decrease in appetite and food intake, even when they feel hungry, due to pain and discomfort associated with eating.
  • Dysphagia: Difficulty swallowing, known as dysphagia, may occur due to the presence of painful ulcers in the mouth, making it uncomfortable to swallow food or liquids.
  • Drooling: Young children with hepatic stomatitis may exhibit increased drooling due to difficulty swallowing and oral discomfort.
  • Fever: A fever may precede the appearance of blisters and ulcers in the mouth, typically occurring 1 to 2 days before the onset of visible lesions.
  • Irritability: Patients, especially children, may become irritable or fussy due to the discomfort and pain caused by oral ulcers.
  • Pain in the mouth: Oral ulcers can cause significant pain and discomfort, making it painful to eat, drink, or speak.
  • Swollen gums: Inflammation of the gums, or gingivitis, may accompany hepatic stomatitis, leading to swollen and tender gum tissue.
  • Ulcers in the mouth: After the blisters rupture, shallow, painful ulcers may develop on the tongue, inner cheeks, or other areas of the oral mucosa.

Diagnosis:

  • History-taking: A thorough medical history, including symptoms and recent exposure to individuals with viral infections, can help in diagnosing hepatic stomatitis.
  • Physical examination: Healthcare providers may perform a physical examination to assess the appearance of oral lesions and other signs associated with hepatic stomatitis.

Treatment:

  • Antiviral therapy: Medications such as acyclovir, an antiviral agent, may be prescribed to reduce viral replication and alleviate symptoms of hepatic stomatitis.
  • Liquid diet: cool-to-cold, nonacidic drinks or soft foods may be recommended to minimize discomfort while eating and drinking.
  • Oral topical anesthetic: For severe pain, oral topical anesthetics like lidocaine may be used to numb the oral mucosa and provide temporary relief. However, caution should be exercised to avoid interference with swallowing and the potential for burns in the mouth or throat.

5. Parotitis

Parotitis refers to the inflammation of one or both parotid glands, which are the largest salivary glands located near the jaw angle.

Causes:

  • Bacterial infection: Parotitis can be caused by bacterial pathogens such as Staphylococcus aureus or Mycobacterium tuberculosis, which may enter the glandular tissue and trigger inflammation.
  • Viral infection: The mumps virus is a common viral cause of parotitis, leading to the characteristic swelling of the parotid glands seen in mumps infection.
  • HIV: Individuals with the human immunodeficiency virus (HIV) may develop parotitis as a result of impaired immune function.
  • Blockage of the parotid duct: Blockage of the main parotid duct or its branches can prevent the normal flow of saliva, leading to glandular inflammation.
  • Systemic infection: Parotitis may occur as a manifestation of a systemic infection affecting the entire body.

Signs and symptoms:

  • Swollen and painful gland: Patients may experience swelling and tenderness in the affected parotid gland, typically observed at the angle of the jaw.
  • Dry mouth: Reduced saliva production due to glandular inflammation can result in dryness of the mouth, leading to discomfort.
  • Severe pain when swallowing: Inflammation of the parotid gland can cause significant pain, particularly during swallowing or chewing.
  • Purulent exudates: In cases of bacterial infection, purulent discharge or pus may be present from the affected gland.
  • Erythema: The skin overlying the inflamed parotid gland may appear red or erythematous.
  • Ulcers: In severe cases, ulceration of the oral mucosa may occur due to inflammation and tissue damage.
  • Fever: Systemic symptoms such as fever may accompany parotitis, especially in cases of infectious etiology.

Diagnosis:

  • History-taking: A thorough medical history, including recent infections, exposure to pathogens, and symptoms, can provide valuable diagnostic information.
  • Physical examination: Enlargement and tenderness of the parotid gland can be observed and palpated during a physical examination.

Treatment:

  • Antibiotics: If a bacterial infection is suspected or confirmed, antibiotic therapy may be prescribed to target the causative pathogens.
  • Mouth washes: Antiseptic or saline mouthwashes may help reduce oral bacteria and promote healing of the inflamed gland.
  • Warm compresses: Application of warm compresses to the affected area can help alleviate pain and reduce swelling.
  • Increased fluid intake: Adequate hydration is important to maintain saliva production and prevent dehydration.
  • Abscess drainage: In cases where an abscess forms within the parotid gland, surgical drainage may be necessary to remove pus and relieve pressure.

Once we have discussed parotitis, let’s now shift our focus to disorders of the esophagus.

Disorders of the esophagus

1. Achalasia 

Achalasia is a neuromuscular disorder of the gastrointestinal tract characterized by the absence of propulsive peristalsis in the esophagus and inadequate relaxation of the lower esophageal sphincter (LES). This condition leads to the accumulation and stagnation of food and fluids in the esophagus, causing irritation and inflammation.

Cause

The exact cause of achalasia is unknown, but it has been associated with degenerative changes or dysfunction in the nerve plexus that innervates the esophageal muscle tissue.

Signs and symptoms:

  • Progressive dysphagia: difficulty swallowing, particularly with solid foods, which worsens over time.
  • Regurgitation of undigested food: Food that is unable to pass through the LES may be regurgitated back into the mouth.
  • Weight loss: due to inadequate intake of nutrients as a result of swallowing difficulties.
  • Halitosis: a foul breath odor caused by the regurgitation of previously ingested food.
  • Coughing when lying down: Irritation of the esophagus may lead to coughing, especially in a horizontal position.
  • Chest pains: Patients may experience chest discomfort or pain, which may worsen after eating.

Diagnosis:

  • Barium swallow: radiographic imaging showing dilatation of the esophagus and lack of peristalsis.
  • Esophagoscopy: endoscopic examination revealing dilatation of the lower esophageal sphincter, as well as potential complications such as esophageal cancer or candida infection.
  • Esophageal manometry: measurement of muscle contractions in the esophagus during swallowing, indicating failure of LES relaxation and lack of peristalsis.
  • Biopsy: Tissue sampling during endoscopy may show hypertrophied muscles and absence of certain nerve cells in the mesenteric plexus, which controls esophageal peristalsis.

Treatment:

  • Pneumatic dilation is a non-surgical procedure involving the insertion of a balloon into the esophagus to stretch the narrowed area and improve swallowing function.
  • Medication: Calcium channel blockers (e.g., nifedipine) and nitrates (e.g., nitroglycerin) may be prescribed to relax the LES.
  • Balloon (pneumatic) dilatation: Similar to pneumatic dilation, this procedure aims to dilate the esophagus at the point of narrowing using a balloon inserted inside the LES.
  • Surgery: Heller myotomy or cardiomyotomy involves surgical division of the muscles at the lower end of the esophagus to relieve the pressure and improve swallowing function.

2. Gastroesophageal reflux (GER)

Gastroesophageal reflux (GER) is a condition characterized by the backward flow of gastric or duodenal contents into the esophagus, occurring independently of vomiting or belching. It results from abnormalities in the barrier between the stomach and the esophagus, often involving abnormal relaxation of the lower esophageal sphincter (LES) and anatomical abnormalities such as hiatus  hernia, where the upper part of the stomach and the LES move above the diaphragm.

Predisposing factors 

Various predisposing factors contribute to GER, including obesity, Zollinger-Ellison syndrome, pregnancy, smoking, hypocalcemia, certain foods (e.g., caffeine-containing beverages, chocolates, spicy and acidic foods), alcohol consumption, large meals, certain medications (e.g., anticholinergics, calcium channel blockers, nitrates), systemic sclerosis, and prolonged nasogastric tube placement.

Signs and symptoms

Common signs and symptoms of GER include heartburn (a burning sensation behind the breastbone, typically occurring after meals), chest pain radiating to the neck and throat, dysphagia (difficulty swallowing), odynophagia (painful swallowing), excessive salivation (water brash), nausea, nighttime coughing, hoarseness, wheezing, belching, and flatulence.

The diagnosis of GER

Diagnosis of GER often involves esophagoscopy to examine the esophagus for damage, barium swallow to evaluate esophageal damage, continuous esophageal pH monitoring to assess acid reflux severity, esophageal manometry, and stool occult blood test to detect bleeding from esophageal irritation.

Treatment strategies

Treatment strategies for GER include lifestyle modifications such as avoiding trigger foods, losing weight if obese, elevating the head of the bed, avoiding lying down after meals, and quitting smoking. Antacid medications like magnesium trisilicate help neutralize stomach acid, while proton pump inhibitors (PPIs) and H2 antagonists like omeprazole and cimetidine, respectively, reduce acid production. Surgical interventions such as Nissen fundoplication (to repair the LES)  and vagotomy (to remove vagus nerve branches innervating the stomach lining) may be considered in severe cases or when conservative measures fail to provide relief.

3. HICCUP

Hiccup, also known as hiccough, is an involuntary contraction of the diaphragm that occurs repeatedly, resulting in a sudden closure of the glottis and a distinct sound.

Causes

  • Hiccups can be caused by various central and peripheral nervous system disorders, often due to injury or irritation to the phrenic and vagus nerves, as well as toxic or metabolic disorders.
  • Triggers include chemotherapy, ingestion of carbonated beverages, alcohol, or spicy foods, prolonged laughter, and eating too fast.

Treatment

  • Ordinary hiccups typically resolve on their own without medical intervention.
  • Anecdotal remedies include startling the affected person, consuming peanut butter or vinegar, drinking water, holding one’s breath, or altering breathing patterns.
  • In severe and persistent cases (“intractable” hiccups), medical treatment may be necessary, including the use of sedatives such as diazepam and chlorpromazine.

Conclusion

With the discussion on hiccups concluded, we will now proceed to explore conditions affecting the stomach. Before we delve into that, let’s review the common manifestations of gastrointestinal tract (GIT) disorders and their management.

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Health assessment | Nursing

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Introduction

Health assessment involves gathering comprehensive data or information from the patient. It is essential that the information collected is thorough and complete. Within this topic, we will explore:

  • History taking
  • Physical examination

History taking

History-taking, also known as a “clinical interview,” is a fundamental aspect of health assessment. It serves as the initial step in understanding the reason for the patient’s visit to the healthcare facility. This structured conversation is designed to uncover the client’s health needs and issues. Typically, it is conducted prior to the physical examination.

During history-taking, it is important to gather the following information:

  • Demographic data, including age, sex, address, and marital status.
  • Presenting complaints.
  • History of presenting illnesses and previous illnesses.
  • Treatment history.
  • Family history.
  • Social and occupational history.

Now, let’s delve into each piece of information that should be collected during history in detail. Demographic data, also referred to as biographical data, encompasses the following information that needs to be collected and documented:

When collecting demographic data or biographical information, it is essential to gather and record the following details:

  • Full name of the client.
  • Age of the client.
  • Gender or sex of the client.
  • Residential address of the client.
  • Marital status of the client.
  • Next of kin, including their relationship to the client and their contact information.
  • Religion of the client.
  • Denomination (if applicable) within their religious affiliation.
  • Nationality of the client.
  • Tribe or ethnic group to which the client belongs.
  • Occupation or employment status of the client, including details about their job role or profession.

The presenting complaint

The presenting complaint is the primary issue that prompted the patient to seek medical assistance. It involves defining the main problem and its duration. Understanding the timing and duration of symptomatic events is crucial because the sequence of the illness can offer valuable insights into its underlying pathological process.

It’s common for some patients, particularly the elderly, to have difficulty recalling the exact duration of their illness. In such cases, they may use significant events as reference points for timing. It can be helpful to inquire about when the patient last felt completely well, as this may jog their memory regarding earlier symptoms that they might have initially dismissed as insignificant.

Obtaining the history of the present illness

When obtaining the history of the present illness, encourage the patient to narrate the sequence of events from the onset of the illness. Ideally, allow the patient to recount their experience without interruption. Offer gentle encouragement if the patient appears anxious or hesitant. For patients who tend to be verbose, gently guide the conversation to focus on relevant details.

Some patients may use medical terms without understanding their significance. Encourage these patients to express their symptoms in their own words. If friends or relatives accompany the patient, always address the patient directly. Once the patient has provided an initial overview of their symptoms, inquire about specific aspects to clarify the onset and duration of the main symptoms. Explore whether any symptoms fluctuate or are linked to specific times, seasons, or events in the patient’s life. After comprehending the patient’s narrative, delve into each symptom in detail to gain a thorough understanding of the illness.

Symptom Analysis

Symptoms, such as pain, serve as valuable indicators guiding clinical examination and subsequent investigations to diagnose and treat underlying conditions. In symptom analysis, it is crucial to consider the course of the illness, the reason for presentation, and conduct a thorough review of systems. For instance, when analyzing pain, it is essential to explore the following aspects and ask the client relevant questions:

  • Onset: When did the pain initially manifest?
  • Location: Where is the pain localized within the body?
  • Duration: How long have you been experiencing this pain? When did it first occur?
  • Characteristics: How would you describe the pain? Is it sharp, burning, or tingling? Is it localized, or does it radiate from one area to another?
  • Aggravating Factors: What exacerbates the pain? Does coughing or breathing intensify it?
  • Relieving Factors: Are there any actions or treatments that alleviate or reduce the pain?
  • Treatment: What medications or treatments are currently being administered for the pain?

By thoroughly analyzing each symptom, healthcare providers can gain valuable insights into the nature of the condition, allowing for targeted interventions and effective management strategies.

To aid in recalling the components of symptom analysis, the mnemonic OLDCART can be used:

  • O: Onset of symptoms: When did the symptoms first appear?
  • L: Location: Where is the symptom localized within the body?
  • D: Duration: How long have the symptoms been present? When did they start?
  • C: Characteristics: How would you describe the symptom? Is it sharp, dull, intermittent, or constant?
  • A. Aggravating factors: What worsens or exacerbates the symptom? Are there specific triggers or activities that make it worse?
  • R: Relieving factors: What alleviates or reduces the symptom? Are there any actions or treatments that provide relief?
  • T: Treatment: What medications or interventions are currently being used to manage the symptom?
  • S: Severity: How intense or severe is the symptom? Can it be rated on a scale from mild to severe?

By systematically considering each aspect represented by the mnemonic OLDCART, healthcare providers can conduct a thorough analysis of symptoms, aiding in accurate diagnosis and appropriate management of the patient’s condition.

History of previous illnesses

Reviewing the history of previous illnesses provides valuable insights into the patient’s overall health status. It is essential to document all significant illnesses, surgeries, and injuries from infancy onwards. During this assessment:

  • Inquire about the nature of each illness to assess the likelihood of accurate diagnosis.
  • Ask about the treatments received for previous illnesses to understand the management approach.
  • Explore any prior hospital admissions to gain further understanding of the patient’s medical history.

Additionally, consider the following points when evaluating the history of previous illnesses:

  • Duration and severity of each illness.
  • Any recurring or chronic conditions.
  • Complications or side effects experienced during treatment.
  • Impact of previous illnesses on the patient’s daily life and functioning.
  • Any family history of similar illnesses or medical conditions.

Assessing the family history

Assessing the family history of your client is crucial for understanding the health status of immediate family members and identifying potential genetic risks. By evaluating family history, healthcare providers can:

  • Determine if the client is predisposed to certain conditions that run in families.
  • Note the client’s position in the family and the ages of siblings or children, if applicable.
  • Document the health status, significant illnesses, and causes of death of immediate relatives.
  • Inquire about hereditary disorders within the family.
  • Ask if any family members have experienced similar symptoms.

The social history of the patient

The social history of the patient encompasses their physical and emotional environment, including their home and work surroundings, as well as their habits and attitudes toward life and work. These factors are crucial in assessing the impact of illness on the patient and their family. During the assessment, inquire about the patient’s leisure activities, alcohol consumption, smoking habits, and exercise routine. Understanding these aspects can provide valuable insights into the patient’s lifestyle and potential factors contributing to their health status.

Occupational history

Occupational history is important, as certain occupations may increase the risk of specific health conditions. During the assessment, inquire about the following aspects of the patient’s occupation:

  • Exposure to hazardous substances at work.
  • Number of hours worked per week.
  • Nature of work, including specific job titles such as secretary, director, underground mine worker, street vendor, bartender, shop assistant, or nursery nurse.

Assessing menstrual history

When assessing menstrual history in women, it is important to inquire about various aspects related to menstruation:

  • Last normal menstrual period: Determine the date of the patient’s most recent menstrual period to assess regularity and identify any abnormalities.
  • Menstrual regularity: Ask about the regularity of menstrual cycles, including the usual duration between periods.
  • Amount of flow: Inquire about the typical amount of menstrual flow, such as light, moderate, or heavy bleeding.
  • Dysmenorrhea: Assess whether the patient experiences any menstrual pain or cramping (dysmenorrhea) and its severity.
  • Menstrual tension: Explore whether the patient experiences any emotional or physical symptoms, such as mood changes or bloating, before or during menstruation.
  • History of taking oral contraception: Determine whether the patient has a history of using oral contraceptives or other hormonal contraceptives and inquire about any associated side effects or complications.

Obstetric History

When obtaining an obstetric history from a woman, gather information about her childbirth experiences, including:

  • Number of pregnancies.
  • Types of deliveries (normal or complicated).
  • Health during pregnancy.
  • History of abortions or miscarriages.
  • Status of children (alive or deceased).

Physical Examination

Following the patient’s history, it is essential to conduct a routine physical examination. This process may cause discomfort for the patient due to the necessary undressing. Thus, it’s crucial to reassure and comfort the patient.

During the examination, ensure gentleness and minimize unnecessary exposure and fatigue for the patient. In cases of acute illness, it may be prudent to delay routine examinations and only perform those necessary for initial diagnosis and treatment. Both history-taking and physical examinations are integral components of patient assessment, with each complementing the other in providing comprehensive care.

History and physical examinations

History and physical examinations work together to provide a comprehensive understanding of a patient’s health. A thorough physical examination necessitates a cooperative patient and a serene, warm, and well-illuminated environment. Natural daylight is preferable over artificial light, as it allows for accurate observation of subtle changes in skin color, such as the faint yellow hue of mild jaundice.

Efforts should be made to help the patient relax, irrespective of the circumstances. For a comprehensive examination, the patient may be asked to undress, but they should be draped with a bed sheet or blanket for modesty and comfort. Patients may be permitted to retain their underwear, but it is essential to ensure examination of the buttocks and genitalia as well.

Having a chaperone present is essential during examinations involving male nurses and female patients, as well as during rectal and vaginal examinations. This presence provides reassurance to the patient and safeguards the nurse against potential allegations of misconduct.

Four primary techniques are employed during physical examinations:

  • Inspection
  • Palpation
  • Percussion
  • Auscultation

Let’s delve deeper into each technique, starting with inspection.

Inspection

Inspection involves visually examining a specific part or area of the body to evaluate its normal state or any deviations from the norm. It’s important to note that inspection goes beyond mere observation; it is a deliberate, systematic, and focused process.

During inspection, you must compare what you see with the known, typical characteristics of the body parts being examined. Ensure adequate lighting is available, and position and expose the body parts in a manner that allows for viewing of all surfaces. Additional lighting may be required to inspect cavities accurately.

Palpation

Palpation involves examining the body through touch. Both light and deep palpation techniques provide valuable information regarding various aspects such as masses, pulsations, organ enlargement, tenderness or pain, swelling, muscular spasm or rigidity, elasticity, vibration of voice sounds, crepitus, moisture, and differences in texture.

During practical training, you will discover that different parts of the hand are more sensitive to specific assessments. For instance:

  • The fingertips are used to palpate lymph nodes and assess pulse rate.
  • The backs of the hands and fingers are employed to evaluate temperatures.
  • The palm surface is best suited for detecting vibrations, while the abdomen is ideal for assessing tenderness or detecting masses.

Percussion

Percussion is a diagnostic technique used to produce sounds and gather information about underlying body structures. This technique can be performed directly or indirectly. Direct percussion involves tapping the body with one or two fingers to produce a sound. However, indirect percussion is more commonly used.

In indirect percussion, the middle finger of the non-dominant hand (known as the pleximeter) is placed firmly against the body surface. The tip of the middle finger of the dominant hand (known as the plexor) strikes the distal phalanx or the distal interphalangeal joint of the pleximeter finger. To produce optimal sounds, it’s important to maintain a relaxed wrist and deliver rapid strikes.

The sounds and vibrations produced during percussion are evaluated relative to the underlying structures. Any deviation from expected sounds may indicate an underlying problem. For instance, the typical percussion sound in the right lower quadrant of the abdomen is tympany. Dullness in this area may suggest a potential issue that requires further investigation. Specific percussion sounds of various body parts and regions are discussed in corresponding assessment notes.

Auscultation

Auscultation involves listening to sounds produced by the body to evaluate both normal and abnormal conditions. This technique is typically performed indirectly, using a stethoscope to enhance clarity by blocking out background noise.

The bell of the stethoscope is more adept at capturing low-pitched sounds, while the diaphragm is better suited for high-pitched sounds. Auscultation is particularly valuable for assessing sounds originating from the heart, lungs, abdomen, and vascular system.

Screening Physical Examination Outline

General Assessment:
  • Evaluate the patient’s overall appearance to determine if they appear healthy, unwell, or ill, as well as whether they are well cared for or neglected.
  • Assess your intelligence and educational level.
  • Evaluate the mental state, including cognitive function and mood.
  • Observe facial expressions and emotional states.

Build and posture:

  • Evaluate the body’s build and posture for any abnormalities or deviations from the norm.

Nutritional Status and Body Composition:

  • Assess for signs of malnutrition, obesity, or edema (fluid retention).

Skin Examination:

  • Evaluate skin color for signs of cyanosis (bluish discoloration), pallor (paleness), jaundice (yellowing), or abnormal pigmentation.
  • Note the presence of body hair and any abnormalities.
  • Look for deformities, swellings, or growths on the body.

Vital Signs:

  • Measure temperature, pulse rate, and respiratory rate to assess physiological function.
  • Look for features indicative of endocrine diseases such as hyperlipidemia, acromegaly, or Cushing’s syndrome.

Hair:

  • Note the distribution and texture of hair, as well as grooming practices.

Eyes:

  • Conduct simple tests of visual acuity by comparing one eye against the other.
  • Check for exophthalmos or enophthalmos.
  • Assess for eyelid edema.
  • Observe the conjunctivae for signs of anemia, jaundice, or inflammation.
  • Evaluate the pupils for size, equality, regularity, reaction to light, and accommodation.
  • Assess eye movement for nystagmus or strabismus.
  • Perform an ophthalmoscopic examination of the fundi and ocular chambers.

Face:

  • Check for facial symmetry or asymmetry.
  • Assess jaw movements.
  • Look for rash or features suggestive of endocrine disease or hyperlipidemia.

Nose/Sinuses:

  • Inspect the external nose, nasal mucosa, and septum.
  • Palpate the frontal and maxillary sinuses for tenderness.

Mouth and Pharynx:

  • Assess for breath odors.
  • Inspect the lips for color and eruptions.
  • Check for tongue protrusion and appearance.
  • Examine the teeth and gums, noting the fit of dentures and their usage.
  • Inspect the buccal mucous membrane for color and pigmentation.
  • Evaluate the pharynx for movement of the soft palate and the state of the tonsils.

Neck:

  • Palpate the thyroid gland and cervical lymph nodes.
  • Auscultate the carotid arteries for a pulse.
  • Note the presence of jugular venous distension and the angle of distension.
  • Assess the range of neck movements and neck rigidity.

Upper Limbs:

  • Conduct a general examination of the hands and arms.
  • Inspect the fingernails for clubbing or koilonychia.
  • Assess pulse rate, rhythm, volume, and character.
  • Evaluate the arterial walls of the radial and brachial arteries.
  • Check the axillae for lymph node enlargement.
  • Measure your blood pressure.
  • Assess muscles for wasting and fasciculations.
  • Perform tests for muscle power, tone, reflexes, and coordination.
  • Check cutaneous sensation to exclude root or nerve lesions.
  • Evaluate joint movement, pain, and swelling.

Thorax: anteriorly and laterally

  • Note the chest type and any asymmetry.
  • Inspect the breasts and nipples for size, shape, inversion, rashes, ulceration, and discharge.
  • Observe respiratory movement, rate, depth, and character.
  • Check for dilated vessels.
  • Palpate for the position of the trachea.
  • Palpate for the apex beat and pericardial thrills.
  • Estimate tactile vocal fremitus.
  • Percuss the lungs.
  • Auscultate heart sounds.
  • Estimate vocal resonance and check cervical and axillary lymph nodes.

Posteriorly (patient sitting):

  • Inspect and palpate respiratory movements.
  • Estimate tactile vocal fremitus.
  • Percuss lung resonance.
  • Auscultate breath sounds.
  • Estimate vocal resonance.
  • Note spine movements and deformities.
  • Palpate the cervical glands and thyroid.
  • Look for sacral edema.
  • Note any kyphosis or scoliosis, and assess for tenderness and range of motion of the back.

Abdomen:

  • Inspect for size, distension, and symmetry.
  • Check for movement, scars, and dilated vessels on the abdominal wall.
  • Look for visible peristalsis or pulsation.
  • Observe pubic hair and hernial orifices.
  • Palpate the abdomen for tenderness, rigidity, hyperesthesia, splashing, masses, and organs such as the liver, gallbladder, spleen, kidneys, and bladder.
  • Assess abdominal reflexes.

Rectal Examination:

  • Examine the anus and rectal wall for lesions, inflammation, and sphincter muscles.
  • Note any nodules or abnormalities.
  • Check for occult blood in fecal matter.
  • In males, palpate the prostate gland.

Lower Limbs:

  • Conduct a general examination of the legs and feet.
  • Assess stance, balance, and gait.
  • Look for pedal edema and varicose veins.
  • Evaluate muscles for wasting and fasciculations.
  • Perform tests for power, tone, reflexes (including plantar response), and coordination.
  • Check joints for movement, pain, and swelling.
  • Palpate peripheral pulses and assess the temperature of the feet.

We have now reached the conclusion of this unit. Let’s review what you have learned.

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