Diagnosis is made clinically and confirmed by imaging and lab tests. Treatment involves IV antibiotics, surgical drainage of abscess, and supportive care. Prognosis is good if treated promptly but can progress to sepsis and death if treatment is delayed.
Diagnosis is made clinically and confirmed by imaging and lab tests. Treatment involves IV antibiotics, surgical drainage of abscess, and supportive care. Prognosis is good if treated promptly but can progress to sepsis and death if treatment is delayed.
Diagnosis is made clinically and confirmed by imaging and lab tests. Treatment involves IV antibiotics, surgical drainage of abscess, and supportive care. Prognosis is good if treated promptly but can progress to sepsis and death if treatment is delayed.
Ruth Zerfu Moderator- Dr. filagot OUTLINE • Introduction • Tropical diseases Amoebic liver abscess Hydatid disease Necrotizing skin infections Cancrum oris E.necroticans Pyomyositis Surgically managed splenic problems Surgically managed typhoid Tropical ulcers Mycobacterial ulcers Chagas disease Schistosomiasis • Diagnosis, complications and management Introduction • Principles of surgery in tropical countries are no different from those in the developed countries • Lack of optimum supporting facilities + late presentations • Younger patients + advanced disease + malnourished • Surgical decision making should be well made for effective Tx. TROPICAL SURGICAL DISEASES 1. AMOEBIC LIVER ABSCESS • Pathogen: Entamoeba histolytica • Transmission: Fecal-oral Amebic cysts are excreted in stool and can contaminate drinking water or food • Stages: Cystic- form in which its ingested- resistant against G.acid Vegetative- Trophozoite formation→ proteolytic enzyme secretion→ invasion of intestinal mucosa→ dissemination to target tissues→ Liver, lung, brain → abscess formation Cont’d • Most common cause of liver abscess worldwide • Multiplication→ blockade of small intrahepatic portal radicles→ focal infarction of hepatocytes + proteolytic liver parenchyma destruction • Variable sizes, single or multiple • Most common location- superior-anterior aspect of the right lobe of the liver near the diaphragm • Contains necrotic center with a thick reddish brown pussy material Clinical features • Intestinal amoebiasis • Loose, bloody stools • Painful defecation, tenesmus, cramps • Fever-10-30% • Extraintestinal amoebiasis • Acute in onset most cases,Liver-95%, rarely lungs and brain • Fever-85–90% • RUQ pain or pressure sensation, hepatomegaly • Chest pain, pleuralgia • Diarrhea- preceeds in 33% of liver abscess cases Management • CBC- leukocytosis • Serum studies- mildly elevated AP is the most common biochemical alteration • fluorescent antibody test- most sensitive • Imaging- abdominal U/S, CT- extra hepatic involvement • well-defined low-density round lesions + enhancement of the wall + peripheral edema • Tx- 1. Medical with Metronidazole 750 mg TID for 7-10 days → abscess may take 30-300 days to resolve • Must be followed by U/S and CT for resolution 2.Surgical Aspiration & drainage- rare • Medical intractability, large abscess, superinfected • If left lobe is involved→ risk for rupture into the pericardium 2. HYDATID DISEASE • Tapeworm- Echinococcus granulosus, E.multilocularis • Definitive hosts- Foxes, dogs, cats • Intermediate hosts- sheep, goats, humans • Cysts contain scolices→ mature in the definitive host→ shed ova→ ingested ova contain chitinous envelope dissolved by G. Juice→ burrows through intestinal mucosa→ portal venous system → LIVER→ mature into adult cyst • Some may bypass the liver into the pulmonary capillary bed or systemic circulation→ Lung (25%), spleen, brain, bones Cont’d • Location- right lobe of the liver, usually the anterior-inferior or posterior-inferior segments mostly single hepatic cyst • Clinical presentation • Uncomplicated cysts are mostly incidental findings • Hepatomegaly- RUQ pain→ single cyst- E.granulosus • Malaise, nausea, vomiting • Chest pain, cough, dyspnea, hemoptysis → infiltrative growth →E.multilocularis • Cyst may rupture→ anaphylactic shock MANAGEMENT • Confirmed via ELISA and U/S • Imaging- 1. Ultrasound Cystic echinococcosis: unilocular, anechoic, smooth, well-defined hepatic cyst with or without daughter cysts Eggshell calcifications within the wall of a hydatid cyst may be visible Alveolar echinococcosis: lesions with irregular, poorly defined margins, central necrosis, and irregular calcifications within the cyst and cyst wall 2. CT scan: indicated for further evaluation of cysts Alveolar echinococcosis usually not well-defined, but shows infiltration of the liver and surrounding tissue evaluating extrahepatic cysts 3. MRI: for daughter cyst characterstics Treatment • Observation: inactive cyst withheterogeneous hypoechoic/hyperechoic contents, or solid, calcified wall • Medical therapy: may be considered as the sole treatment for cysts < 5 cm • Drug of choice: albendazole • U/S or CT-guided percutaneous drainage • Commonly conducted using the PAIR (puncture, aspiration, injection, reaspiration) procedure • Should only be done in combination with medical therapy • Indications: > 5 cm and/or septations • Surgery • Goal: resect the whole cyst to prevent spillage of its content • Indications: > 10 cm, complicated cysts • Follow-up: Because relapse is common, patients should be closely monitored via imaging for up to five years NB. Caution not to rupture cyst wall→ protoscolice spillage 3.Necrotizing soft tissue infections • Aggressive, life threatening infection with necrosis of tissue • Cellulitis, fasciitis ,myositis • Fasciitis is the most common • Necrotizing fasciitis: rapidly progressive infection of superficial and deep fascia- life threatening within hours Fournier gangrene: NF of the external genitalia with rapid spread to the anterior abdominal wall and gluteal muscles Clostridial myonecrosis: C.perfringes & C.septicum Etiology • Both polymicrobial and monomicrobial Polymicrobial - aerobic+ anaerobic- mostly of GI and GU origin E.coli, bacteroides Monomicrobial- GAS, S.aureus • Fourniers gangrene- mixed with facultative bacteria( E.coli, klebsiella, Enterococcus) and anaerobic bacteria Clinical features • Systemic symptoms: Fever, chills, altered mental status • Cutaneous findings • Diffuse erythema (often manifests initially as suspected cellulitis that is not responding to initial antibiotic) • Extreme tenderness and pain out of proportion to the area of erythema • Significant induration of the SCT • Crepitus: due to the production of methane and CO2 by bacteria • Purple skin discoloration skin necrosis and ecchymosis • Bullae • Loss of sensation in the affected area (paresthesias) • Definitive diagnosis is usually made during the visualization of the tissue during surgery Management • CBC- leukocytosis • Inflammatory markers- CRP, ESR, procalcitonin • CK levels • Blood cultures • Imaging- CT/MRI with or without IV contrast, U/S and X-ray • Gas in soft tissue • Fascial thickening and edema • Lack of contrast- indicates necrosis • N.B. Surgical exploration and empiric AB therapy must not be delayed for such extensive studies Cont’d • If the presentation of the patient is highly suspicious for NSTI
Admit the patient immediately and consult ICU for possible septic features
Empiric antibiotic therapy and surgical exploration
• Extensive and necrotic tissue must be debrided + • Samples must be sent for gram staining + • Re-exploration every 12-36 hrs for necrotic tissue Cont’d • During surgical exploration, if the tissue is necrotic: • Fascia appears swollen • Dull gray fascia • Possible brown exudate • Easy dissection of tissue planes with a blunt instrument or gloved finger • In antibiotic treatment: Start systemic, broad-spectrum antibiotic therapy immediately after blood cultures have been obtained • consider polymicrobial causes 3a.Cancrum oris ( gangrenous stomatitis) • Necrotizing infection of the mouth, nose and lips • Children are commonly affected-HSV,scarlet fever,TB • Begins as an ulcer→ at alveolar margin of the mouth and rapidly spreads to involve the teeth, jawbone, cheek, tongue, lips, and nose • Necrophorum and Prevotella intermedia in children and pseudomonas aerugiosa in neonates Cont’d • Risk factors Malnutrition- vital factor Bacterial infections Poor environmental sanitation Poor oral hygiene Frequent exposure to human/animal feces Prior history of viral or bacterial infection Immunodeficiency • Clinical features • ulcer formation • include swollen gums • swollen cheek lining Cont’d • Diagnosis • inflamed mucus membranes, oral cavity ulcers, and skin ulcers- must be explained in detail during medical history • X-ray • MRI • CT of the jaw, neck and head • Blood cultures and biopsy • Blood test- to check for immune system functioning Treatment • If not treated severe facial disfiguration, sepsis and pneumonia are common complications • Systemic antibiotics+ appropriate nutritional support + hydration and proper electrolyte balance • Surgical treatment: offered for debridement of affected tissue and facial reconstruction 4. Pyomyositis (myositis tropicans) • Definition: purulent infection of skeletal muscle • In the tropics occurs mostly without penetrating trauma or spread from an adjacent septic focus • 95% S.aureus, others include S.pyogenes, E.coli • Risk factors: chronic ill health and debility trauma producing muscle haematoma Filariasis Skin infections Dracunculus infection( guniea worm infection) malaria and viral myositis Immunocompromised state (HIV) Cont’d • M>F, affects the bulky muscles of the lower extremities commonly • Clinical features • Stage 1 Cramps and aches of affected muscle Low grade fever • Stage 2 Abscess has formed 90% are diagnosed in this stage Fever,chills, lump under the muscle and mobility issues Cont’d • Stage 3 • Septic shock • High fever • End organ damage • Diagnostics: • Ultrasound guided pus aspiration • Physical examination- mobility issues, pain sensitivities, abscess • Blood studies- leukocytosis • Imaging- MRI- best modality for visualizing and characterizing the abscess Treatment • Antibiotics+ if there is an abscess- drainage 5. Enteritis necroticans( pig bel) • ‘Pig-Bel’ in the highlands of Papua New Guinea (PNG) • Rare disease associated with children and diabetic patients • following a feast of pig meat and sweet potato • Beta-toxin producing C.perfringens type C are associated with the disease • concurrent ascaris infection→ prevents gut destruction of the toxin • Clinical presentation: abdominal pain, distention, vomiting, and passage of bloody diarrhea Cont’d • The infection might also lead to shock, obstruction and malnutrition if untreated • Treatment: • restoration of fluid and electrolyte imbalance by intravenous therapy • nasogastric decompression • Antibiotics • IV penicillin • If there is no improvement→ laparotomy with resection of the gangrenous bowel segment • Prevention- toxoid vaccine (PNG) along with the DPT vaccine