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MEDICINE ROTATION WEEK 8 Student Name: Student ID: MUBARAK HOSPITAL Date: 31/10/2012 1 Personal Details Name: Mr. N.A Age: 53 years Marital status: Married Occupation: Secretary Residence: Flat, 2nd floor, no elevator Ethnicity: Egyptian, Muslim Presenting Complaint 3 days H/O 1) Generalized abdominal pain and distention 2) Nausea 3) Fever 4) Diarrhea History of Presenting Complaint MR. N.A, a known case of HCV with chronic decompensated liver cirrhosis, is a 53 years old Egyptian gentleman who presented to the Casuality Department on 29/10/2012 with a 3 days history of abdominal pain and distention, nausea, diarrhea and fever. The abdominal pain was sudden in onset, progressive and continuous in nature, diffuse, colicky in character and non-radiating. It was rated as 10 in terms of severity on a scale of 1-10. There were no aggravating or relieving factors. Concerning the fever, it was intermittent, high grade (up to 39) and associated with chills and rigors. As for the diarrhea, the stool was noted to be watery, non-fatty, non-bloody, and with no mucus or discharge. Associated symptoms were anorexia and loss of appetite otherwise the patient gave no H/O vomiting, constipation, hematemesis, dyspepsia, dysphagia, weight loss, drowsiness, cough, dysuria or hematuria.Upon further questioning, the patient revealed H/O stopping his medications (aldactone) because of not feeling well. The patient is known to have DM type 2 and is on treatment (insulin) with no micro or macro-vascular complications. Past Medical History H/O HCV+ decompensated chronic liver disease– 10 years, on aldactone 50 mg PO OD, follows up with gastroenterologist in Egypt. H/O DM Type 2- 7 years, compliant on insulin mixtard 80 units/day, follows up in Egypt. No H/O HTN No H/O hyperlipidemia No H/O asthma No H/O cardiac disease or other significant illnesses No H/O past surgeries/ procedures No H/O previous hospitalizations/ICU admissions. 2 Family History Father Passed away; no significant medical history Mother Passed away; no significant medical history Siblings 2 brothers, 3 sisters all alive and well. Children 3 children, alive and well. Family No significant illness in family No H/O condition similar to patient’s condition Drug History Aldactone 50 mg PO OD Losec 20 mg PO OD Insulin mixtard 80 units/day Social History Tobacco: Non-smoker Alcohol: Non-ethanol consumer Life style: Sedentary, lives with his family. Stress: None. Travel: No history of recent travel. Pets: None. General Health Status Appetite: Decreased Weight: 80 kg, constant. Height: 175 cm. Bowel habit: Mentioned above. Micturation: Regular, no obstructive/irritative urinary symptoms, no haematuria, light yellow urine. Sleep: Normal. Energy: Decreased Well being: Unsatisfactory 3 Systems Review Alimentary Mentioned above Respiratory No H/O, cough, wheeze, haemoptysis, night sweats, or fatigue Cardiovascular No H/O palpitations, syncope, orthopnea, paroxysmal nocturnal dyspnea Urogenital Normal stream and frequency, no H/O urgency, hesitancy, dysuria, intermittency, hematuria, or post-micturation dribble Joints/muscles No limitation, painful movement, swelling, joint deformities or stiffness Neurological No H/O drowsiness, numbness, tingling , syncope, seizures, headaches, balance and coordination normal, no dizziness or vertigo Special Senses: Normal hearing, normal vision, normal smell, normal tasting. Physical Examination The patient was alert, cooperative, responsive, well oriented to time, place and person, and lying down comfortably in bed. Vital Signs Heart Rate: Blood pressure: Respiratory: Temperature: SpO2: 80/min 124/80 mmHg 15 /min 37.4 oC 98% General Inspection General Normal, not in respiratory distress (no use of accessory muscles of breathing) Hands Palmar erythema otherwise no evidence of color abnormality like peripheral cyanosis /tobacco staining, no nail abnormality like clubbing/ koilonychias/leukonychia/splinter hemorrhage, no joint abnormality, no hand deformity like ulnar deviation/dupuyten’s contracture, no muscle wasting, flapping tremor or bounding pulse,Normal Temp. of both hands (RT=LT). Eyes: Conjuctival pallor and scleral jaundice Mouth: No evidence of mucosal cyanosis, no evidence of oral ulceration, patient has normal teeth, no evidence of tongue abnormality like wasting/enlargement/ inflammation/discoloration/abnormal movements. Neck Spider nevi – otherwise no evidence of distended neck veins or parotid gland enlargement Muscles/joints No swelling or deformities, no evidence of erythema, or rash 4 Alimentary System Inspection: Hands: Palmar erythema, otherwise no clubbing, duputeryns contracture, muscle wasting or flapping tremor. Eyes: Jaundice and pallor, no xanthelasmas Mouth: Clean mouth, normal breath. Neck: 2 spider nevi, otherwise no dilated veins or parotid gland enlargement. Chest: Gynecomastia, spider nevi >4, otherwise no dilated veins and chest moves symmetrically with respiration Abdomen: Abdomen is distended, umbilicus is everted, visible dilated vein, hair loss, otherwise no scars or stomas on abdominall wall, no rashes, striae or bruising. Leg: No lower limb edema. Palpation: Abdomen is distended Superficial palpation: Minimal tenderness, no guarding or rigidity Deep palpation: No masses or organomegaly felt. Liver span: Normal -10 cm Spleen: Palpable spleen Shifting dullness positive Fluid thrill negative Auscultation: Positive bowel sounds, no bruits heard over liver or aorta. Auscultation of chest: normal breath sounds over both lung fields, no added sounds Hernia: None detected in groin, scrotum or central abdomen. Rectal exam: Not performed. Respiratory System Trachea: Central. Inspection: Normal chest shape, symmetrical, elliptical in cross section, no evidence of any deformities like kyphosis/scoliosis/pectus carinatum/ pectus excavatum, no evidence of scars, swellings, subcutaneous lesions or dilated veins on chest wall. Percussion: Resonance over both lung fields (Right = Left). Auscultation: Vesicular breath sounds over both lung fields, no added sounds. Chest expansion: Normal and symmetrical expansion. 5 Cardiovascular system Inspection of chest wall: No scars, obvious veins, bony deformities or obvious pulsations. Radial pulse: Normal volume, regular rhythm, normal character, symmetrical, non-collapsing. Apex: Palpable in the 5th ICS, within the MCL. Auscultation: Normal S1 and S2, no evidence of S3 orS4, added sounds or murmurs. JVP: Not visible. Pulses: Site Right Left Carotid ++ ++ Radial ++ ++ Brachial ++ ++ Femoral ++ ++ Popliteal + + Dorsalis Pedis + + Posterior tibial + + No radiofemoral delay. Auscultation Abdomen: No bruits heard. Femoral: No bruits heard. Inspection of abdomen: No visible pulsation. Palpation of abdomen: Abdominal aorta not palpable. Inspection of right leg: rashes. Normal hair distribution, no ischemic changes, ulcers, swelling, scars or Palpation of right leg: No tenderness, pitting oedema or palpable popliteal artery. Temperature: Normal. Neurological System Cranial nerves: I – IX, XI and XII tested – normal, visual fields normal. Reflexes: Normal and symmetrical in both sides. Planter reflex: Negative. Sensation: Normal and symmetrical in both sides. Motor: Normal and symmetrical in both sides. Power: Normal and symmetrical in both sides. 6 Renal system Inspection: No abdominal distention, suprapubic swelling or scars. Palpation: No enlargement of kidneys/bladder or tenderness. Ballottement: Kidneys not enlarged. Pressure on renal angle: No tenderness. Percussion over suprapubic area: Resonance. Auscultation: No bruits heard. Musculoskeletal Inspection No evidence of swelling, erythema, rash or visible deformities Palpation No pitting edema, change in temperature, tenderness, or effusion detected Movements No restriction in movement Lymph node examination Cervical, axillary and inguinal LNs examined bilaterally – NAD. Neck examination No swellings, masses or deformities were inspected or palpated. Investigations 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. CBC Clinical Chemistry Lipid Profile Mineral Profile Blood film Coagulation profile ECG CXR US abdomen and pelvis αFP Blood C/S Ascitic tap a. WBC & Differential b. Gram stain c. C/S d. Albumin e. Cytology 13. Serum albumin 14. HbA1C 15. 24 hour urine protein 7 16. Fundoscopy 17. UCnI endoscopy 1) CBC Test Result Hb 138 N 130-170 g/L RBC 4.07 L 4.5-5.5 x10^12/L Hematocrit 0.412 N 0.4-0.5 L/L MCV 99.0 N 83-101 fL MCH 33.9 H 27-32 pg RDW 17.9 H 11.6-14 % Platelet count 35 LL 150-410 x10^9/L WBC 15.9 H 4-10 x10^9/L Neutrophils 8.3 H 1.7-7.5 Lymphocytes 0.7 L 1-3 Monocytes 0.7 N 0.2-1 Eosinophils 0.0 L 0.02-0.5 Basophils 0.0 L 0.02-0.1 Normal value Evidence of low platelet count indicating thrombocytopenia possibly due to liver cirrhosis. Evidence of leukocytosis mainly Neutrophils indicating underlying bacterial infection 2) Clinical Chemistry Test Result Normal value Gluc 7.2 H 3.9-6.1 mmol/L BUN 3.4 N 2.5-7.1 mmol/L Urea 3.4 N 1.5-6.6 mmol/L Creat 67 N 62-115 umol/L Na 136 N 136-144 mmol/L K 4.3 N 3.6-5.1 mmol/L CO2 28 N 22-32 mmol/L Albumin 32.0 L 35-47 g/L Cl 104 N 94-115 mmol/L LDH 162 N 90-180 IU/L Alk. Pho 140 H 26-88 IU/L ALT 17 N 10-60 IU/L AST 18 N 10-42 IU/L 8 GGT 35 N 7-64 IU/L Evidence of slightly low albumin suggestive of underlying chronic disease or malnutrition. 1) Blood C/S Awaiting results. 2) Sputum C/S Awaiting results. 3) ESR/CRP Test Result Normal value ESR 14 N 0-20 m/hr 4) Urine R/M C/S Awaiting results 5) ABG Test Result Normal value pH 7.351 7.35 – 7.45 PO2 11.78 kPa 10.67 – 13.33 kPa PCO2 5.74 kPa 4.67 – 6.00 kPa HCO3- 24.0 mmol/L 24 – 26 mmol/L Normal 6) CXR Hetereogenous opacity over right upper lobe suggestive of right lobar pneumonia 7) ECG 9 Working Diagnosis and Management Plan From the patient's history and clinical examination of the chest, a diagnosis of Spontaneous Bacterial Peritonitis in a case of chronic decompensated liver disease was made. A management plan was set up for the patient and the patient was managed accordingly with: 1. Close observation of vital signs 2. Order the following investigations: a. b. c. d. e. f. g. h. i. j. k. l. CBC Clinical Chemistry Lipid Profile Mineral Profile Blood film Coagulation profile ECG CXR US abdomen and pelvis αFP Blood C/S Ascitic tap i. WBC & Differential ii. Gram stain iii. C/S iv. Albumin v. Cytology m. Serum albumin n. HbA1C o. 24 hour urine protein p. Fundoscopy q. UCnI endoscopy 3. Low salt, diabetic diet 4. Administer: a. Aldactone 50 mg PO OD b. Losec 20 mg PO OD c. Claferan 1 gm IV TDS d. Insulin actrapid 8 8 8 e. NPH 10 10 Based on the results of the investigations (mentioned above) of a diagnosis of Spontaneous Bacterial Peritonitis in a case of chronic decompensated liver disease was made. 10 Summary-in-the-box Spontaneous bacterial peritonitis (SBP) is the development of peritonitis (infection in the abdominal cavity) despite the absence of an obvious source for the infection.[1] It occurs almost exclusively in people with portal hypertension (increased pressure over the portal vein), usually as a result of cirrhosis of the liver.[1] It can also occur in patients with nephrotic syndrome. Symptoms include fevers, chills, nausea, vomiting, abdominal tenderness and general malaise.[1] Patients may complain of abdominal pain and worsening ascites.[1] Thirteen percent of patients have no signs or symptoms.[5] Hepatic encephalopathy may be the only manifestation of SBP; in the absence of a clear precipitant for the encephalopathy, all patients should undergo paracentesis, or sampling of the ascites fluid, in order to assess for SBP. SBP is thought to result from a combination of factors inherent in cirrhosis and ascites, such as prolonged bacteremia secondary to compromised host defenses, intrahepatic shunting of colonized blood, and defective bactericidal activity within the ascitic fluid.[6] Contrary to earlier theories, transmucosal migration of bacteria from the gut to the ascitic fluid is no longer considered to play a major role in the etiology of SBP.[7]With respect to compromised host defenses, patients with severe acute or chronic liver disease are often deficient in complement and may also have malfunctioning of the neutrophilic and reticuloendothelial systems.[8]As for the significance of ascitic fluid proteins, it was demonstrated that cirrhotic patients with ascitic protein concentrations below 1 g/dL were 10 times more likely to develop SBP than individuals with higher concentrations.[9] It is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the protein concentration.[10] Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.[ Diagnosis necessitates paracentesis (needle drainage of the ascitic fluid) and laboratory confirmation of ascitic neutrophils > 250/mm³. After confirmation of SBP, patients need hospital admission for intravenous antibiotics (most often cefotaxime 2g IV Q8-12H for at least 5 days or ceftriaxone 2g IV Q24H). They will often also receive intravenous albumin. A repeat paracentesis in 48 hours is sometimes performed to ensure control of infection. Once patients have recovered from SBP, they require regular prophylactic antibiotics as long as they still have ascites.A randomized controlled trial found that intravenous albumin on the day of admission and on hospital day 3 can reduce renal impairment.[11] My references: Davidson's principles and practice of medicine, 21st edition. Oxford clinical medicine, 7th edition. 11