I present actual cases using the Problem Oriented System (POS), in a simplified format to illustrate the use of problem list, assessment and plan in tabular format. I posed questions for the reader; in the subsequent month I provided answers which are located in brackets '[....]' and in the 'answers' text. NOTE: The following Cases were included in my prior HomePage 1996 to 1999.

Case Archives (case reports, questions (?) and answers[....] )
#12 3/22/99
#11 1/25/99
#10 10/18/98
#9 8/10/98
#8 4/30/98
#7 2/15/98
#6 12/17/97
#5 10/25/97
#4 9/3/97
#3 6/15/97
#2 2/20/97
#1 12/10/96

"The text contains English language phrases used only in Japan."
>Could you please list some examples?

1. Chest x-p = chest x ray
2. 8.9° = 38.9°
3. Rehabili = rehabilitation
4. FGS = endoscopy
5. FCS = colonoscopy
6. FBS = bronchscopy
7. BW = weight
8. BT = temperature
9. UCG = Echocardiogrqam
10. Abdominal Echo = ultrasound
11. Defense = guarding
12. AP = angina
13. MK = magen krebs(german) = gastric ca
14. MT= magen tube(german) = naso gastric tube



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Case #12 3/22/99
45 yo woman home maker
cc: fever & sore throat
HPI: 6 weeks prior to admission(PTA), patient developed a 'common cold' with fever to 39° and severe sore throat. Her local physician prescribes a penicillin antibiotic; she developed a rash and painful elbows & knees 10 days later. Her fever, non-pruritic rash and joint pains continued. 7 days PTA she developed swollen knees and ankles. When seen in clinic 1 week later, she was admitted. 
PMH np. ROS wt loss 2 kg/2months, no cough, sputum, conjunctivitis, urinary symptoms.

PE BP 134/70, HR 78, RR 14, 38.5°, BMI 17.6, conjunctivae pallor, morbilliform eruption on trunk, arms, legs not face, palms, soles; R cervical 1 cm non tender, non-fixed firm lymph node; systolic flow murmur, liver edge +/-, OB (-) x 3. 
Lab WBC 8500, Hb 9.3, MCV 84, GOT/GPT, electrolytes, renal tests,blood sugar np, CRP 2.3, ESR 70, INR 1.25, aPTT 27, platlets 320,000, U/A np;chest xp, plan abdominal, ankle, knee films np; ECG np; C'3 109(50-70) C'436(15-30), Fe 25, UIBC 300, RF/ANA np, ferritin 4500, Fiber gastroscopy: multi-gastric erosions, skin patch tests with penicillins np.

Hospital course: After one additional month of observation with continued symptoms, a medication was started which relieved her symptoms.

Questions for Case # 12
1. What is your differentail diagnosis for sore throat, arthralgias/arthritis, rash, lymphadenopathy?
2. What additional tests might be planned for Assessment # 1 ?
3. What additional tests might be planner for fever assessment ?
4. With normal results of the planned tests for anemia, what is the likely cause of her anemia?
5. What screening tests should be ordered to rule out cancer?
6. Assuming no additional tests made a specific diagnosis, what is the probable diagnosis and what medication caused her symptoms to resolve.

Answers for case # 12
1. STAR syndrome(Sore Throat, Arthritis & Rash) diagnosis is determined by duration: Less than 3 weeks consider viral causes such as parvovirus and serum sickness; 3-6 weeks consider acute rheumatic fever; over 6 weeks consider adult Still's disease
2. For diseases less than 3 weeks: other penicillin components for skin tests, viral titers for parvovirus, echovirus, adenovirus, coxsackie virus; more than 3 weeks ASLO titer.
3. Blood, urine, induced sputum cultures; sputum and skin test for Tb; consider lymph node biopsy if node increases in size.
4. She received oral iron with no change in Hb after 1 month. Consider the anemia of chronic disease.
5. Cervical Pap cytology, mammography, colonoscopy and repeat gastroscopy with biopsy.
6. My diagnosis is adult Still's disease because the 1)ferritin was higher than acute phase reaction and 2) she responded dramatically to aspirin.

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Case #11 1/25/99
19 yo male college student
cc: chest pain and dyspnea
HPI: 17 days prior to admission(PTA), patient developed a common cold. 10 days PTA patient fell down flight of steps for unkown reason, sustaining hitting his chest, without head injury, causing immediate chest pain(CP). 7 days PTA he went to a local hospital because of continuous CP where treatment was not helpful. 3 days PTA he had increasing dyspnea and orthopnea. His progressive symptoms resulted in visiting the teaching hospital where he was admitted.
PMH np. ROS no other complaints.

PE BP 128/86, RR 40, 37.5°, pulse 115, [no description of JVD, chest wall tenderness], lungs clear, heart np, remainder of PE np.
Lab WBC 16,800, Hct 40, GOT/GPT 78/113, electrolytes, renal tests,blood sugar np, CRP 10, CK/CK MB 76/12, chest xp increased cardiac sulhouette with 71% CTR, ECG sinus tachycardia 115, elevated ST segments in leads 2,3, AvF, V2-5, T waves all upright, cardiac ECHO 10 mm circumferential pericardial effusion, with anterior septal hypokinesis.

Hospital course: Without any special treatment, the student gradually improved and was discharge after 2 weeks of hospitalization.

Questions for Case # 11
1. How is cardiac tamponade diagnosed?
2. What are types of traumatic heart disease?
3. Is CHF present?
4. What diagnosis is made from the ECG?
5. What are possible reasons for cardiac ECHO showing anterior septal hypokinesis?
6. Why is troponin test helpful?

Answers to case # 11
1. The clinical signs are increased JVD, paradoxical pulse which are not specific. But when present with postive cardiac ECHO findings, then tamponade is likely. The ECHO finding are, in addition to the pericardial effusion, right atrial or ventrical diastolic collapse. Reduced Doppler inflow velocity during inspiration across the mitral valve also supports the diagnosis. Data is missing to make this diagnosis. I suspect it was present.
2. From blunt trauma: to myocardium, possible contusion, laceration, hemopericardium and tampomade; to pericardium, possible pericarditis, bleeding; to endocardium possible rupture of papillary muscle and valves; to coronary arteries possible thrombosis.
3. Probably the usual forms of CHF with systolic and/or diastolic failure are not present. I suspect increased vena cava pressure from the tamponade caused back pressure to the liver resulting in mild enzyme elevation.
4. Pericarditis is suspected because of the diffuse ST segment elevation with concordant upright T waves. This traumatic presumed bloody effusion causes inflammation. Probably true myocardial infarction did not occur but it might have.
5. I suspect the hypokinesis represented contusion to the myocardium with possible mild inflammation.
6. The new troponin test for myocardial damage remains abnormal for 10 days. Hence the abnormal test would support the diagnosis of myocardial damage from either the contusion or infarction.

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Case #10 10/18/98

39 yo woman
cc: lower extremity edema with pain
HPI: One week before admission pt delivered normal infant vaginally with no complications. 2 days before admission pt developed acute left lower extremity swelling and pain. 1 day before admission pt seen in ER by orthopedic physician who found no fractures and sent the pt home. The pt returned to ER because of continued symptoms and was admitted to general medicine.
PMH: History of leg swelling and pain with pregnancy 11 years earlier
ROS: Serous vaginal discharge; no injury to leg; no dyspnea, chest pain.
PE 120/70, P 72, BT 37.5°, RR 20; lungs clear; midline lower abdominal tenderness without guarding; left entire lower extremity edema from upper thigh to toes, with diffuse tenderness, gait disturbance from leg pain, Homan sign (-); digital rectal examination: + uterine tenderness & stool occult blood (-).
Lab: WBC 8,800, Hmb 11.8, plat 252,000, PT 11.1, aPTT 28, arterial Sat O2 99%, U/A np, CRP 2.3; Chest x-p np; ECG np; lower extremities Doppler(+) for DVT.

Hospital course: Heparin was given for adjusted aPTT ~ 60 seconds for 5 days and warfarin was started shortly after heparin to an adjusted INR 2-3. The lower extremity edema resolved slowly over 3 weeks. Gait returned slowly to normal. Blood cultures were negative. Spiral abdominal and chest CT were negative.

Questions for Case # 10
1. Why did the orthopedic physician not diagnose DVT?
2. What additional tests are helpful to diagnose DVT & pelvic phlebitis?
3. How soon after the diagnosis of DVT should heparin be started?
4. How is endometritis diagnosed?
5. Which antibiotics are indicated for endometritis?
6. Which hypercoagulation disorders are most likely for this pt?
7. Which hypercoagulation studies are indicated?

Answers for case # 10
1. Many orthopedic residents have poor clinical training especially in the area of general medicine. In America if the patient had had complications from the missed diagnosis of DVT such as pulmonary embolism(PE) and died, it would be medical malpractice.
2. D dimer, Doppler ECHO of pelvic veins; for spiral CT seeRadiology 1998;208:201-208.
3. When thinking of reasonable possibility of PE, start heparin at once before diagnostic studies completed
4. Pelvic examination showing uterine tenderness, discharge and fever.
5. Cefoxitin & clindomycin when onset < 48 hrs for usual GU and anerobic bacteria; doxycycline for later onset becasue of chlamydia likely.
6. Antiphospholipid syndrome and activated protein C resistance
7. Anticardiolipin antibody and lupus anticoagulant; heparin may cause false (+) lupus anticoagulant; aPTT is a screen test for the presence of the lupus anticoagulant; with and without activated protein C and factor V gene via PCR may also be considered.

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Case #9 8/10/98

78 yo man
cc: pedal edema, anemia
HPI: 8 mos before admission patient admitted for syncope to neurology, no cause found but ECG had ST ^ V1-2, Cardiac ECHO showed localized hypokinesis called DCM with near normal LV(43mm) chamber; anemia noted , Fe deficiency suspected > Fibergastroscope(FGS) np found > oral Fe with good response. 1 month before admission stopped Fe > anemia, 2-3 days before admission acute, severe pedal edema developed. ROS: No dyspnea, chest pain, prior liver, renal problems.
PE 150/60 tilt> 130/80 P 80 > 87; 5 cm +^JVD; S4, systolic M, 4+bilat pedal edema to ankles; Stool occult blood (+ ), stool dark brown color.
Lab: WBC 5,500, Hmb 6.3, Hct 19.1, MCV 95. MCH 31, plat 279,000, BUN / creatinine31/ 0.9, PT 10.3, aPTT 25, ferritin 20, Fe 28, UIBC 333, Sat O2 99%, U/A np; Chest x-p ?Kerley B lines, LV configeration, ? small effusion; ECG ST ^ v2-3(?old, ? aneurysm), q wave AvL, LVH, lower extremities Doppler(-) for DVT.

Hospital course: Treatment: 4 units red cells and lasix improved patient. FCG showed angiodysplasia as bleeding cause.

Questions for Case # 9
1. Why did pt stop taking Fe?
2. Why was FCS omitted first admission?
3. What is significance of + tilt test ?
4. What is mechanism of edema?
5. What urgency level should be considered for OB + anemia needing transfusions?
6. Why is pt assigned to neurology for syncope?
7. What is significance of ST ^ ?
8. What is significance of abnormalities on cardiac ECHO?

Answers for case # 9
1. It is unclear why pt stopped taking Fe. Perhaps he was non-compliant; perhaps his treating physician failed to continue Fe. Usually oral Fe is continued for 4-6 months after GI bleeding with depleted Fe marrow stores.
2. FCS was omitted because of physician error. It should not have been omitted.
3. + tilt test usually means hypovolemia in the absence of autonomic dysfunction.
4. Edema probably represents heart failure
5. Pt's with OB + , tilt test + anemia are hypovolemic and actively GI bleeding; such pt's should be treated urgently with fluids(N/S) followed by transfusions to prevent shock and myocardial ischemia.
6. In the absence of definite neurology signs, pt's should not be assigned to neurology service since cardiac causes dominate as underlying mechanisms of syncope. The best choice of specialty service is general medicine service, which is grossly under-represented in Japanese hospitals usually.
7. ST segment elevation suggests myocardial ischemia needing evaluation for AMI or aneurysm.
8. Cardiac ECHO suggests ischemic heart disease because of localized hypokinese and normal chamber sizes. In DCM chamber sizes are increased, a feature absent in this case.

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Case #8 4/30/98

49 year old woman
cc: blurred vision
HPI: Two days before admission she had visual blurring in both eyes. She took her own BP and noted it was 176/110. On the day of admission she came to eye clinic, bilateral fresh flame- shaped retinal hemorrhages were seen; she was immediately sent to general medicine clinic where her BP was 204/130. She was admitted soon thereafter. PMH Hypertension(H-T) 1 year ago(160/?), never treated. ROS No headaches seizures, chest pains, diabetes. Smokes 30 cigarettes/d

PE 36.5°, 204/130(same both arms, no orthostatic changes), HR 68, RR 12. Fundi (see above), neck no bruits, chest clear, heart np, abdomen no bruits, neuro & mental status exams np. WBC 5,000, Hmb 14.8 , plat 150,000, BUN/Creatinine np, K 4.4, U/A prot -, RBC-, Chest x-p np, ECG np(no LVH).

Hospital course: Treatment controlled her BP to 130/90 by the second hospital day. She was discharged on the third day with continued blurred vision and mild headache.

Questions for Case # 8
1. If there is any target organ damage from her H-T, what organ(s) is it?
2. What type of hypertension ( assessment ) does the patient have?
3. What treatment plan is best for this type of H-T?
4. What is the target BP?
5. In what type of H-T patient should underlying causes of H-T be considered?
6. What is your assessment for secondary H-T causes?
7. What is the plan of studies for this patient if secondary H-T suspected?

Answers for case # 8
1. Retinal flame hemorrhages are considered a sign of central nervous system damage.
2. This is considered a form of H-T emergency because she has H-T encephalopathy as shown by retinal hemorrhages; this may also be considered a form of malignant H-T
3. DIV medication to lower mean arterial BP by 25% over 3-4 hours. More rapid lowering may cause cerebral ischemia. I used a calcium channel blocker nicardipine.
4. Target mean arterial BP = (systolic BP + 2 x diastolic BP)/3= 204 + 2 x 130/3 = 155
5. In any patient presenting with malignant H-T, secondary causes should be assessed.
6. Consider a)renal vascular H-T, b)primary aldosteronism and c) pheochromocytoma
7. a. renal artery ECHO Doppler and/or ACE-I/captopril renal flow scintography b. 24 hour urinary aldosterone during salt loading, c. urinary metanephrine-to-creatinine ratio

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Case #7 2/15/98

75 year old woman
cc: headache and fever
HPI: 1/1/2 years ago she fell in rice field > headache/fever 39° 3-4 months, weight loss, then spontaneously improved. Now, 1 yr later, 1 month fever & headache, home fever 38°, fatigue, malaise. At admission, headache, jaw claudication, shoulder myalgias. PMH H-T 2-3 years, anemia given Fe. ROS jaw claudication with headaches this past month.

PE 37.5°, 150/95, Temporal arteries hard, no bruits, soft systolic flow cardiac murmur, Chest x-p uncoiled aortic arch, ECG np. WBC 13.5 Hct 39, Hmb 13.5 , plat 563,000, ESR 80 , CRP 7.0, BUN/Creatinine nrep, U/A Occult blood +, prot 2+, 10-20 RBC, Ccr 52, prot/24 hr 300 mg, no casts in U/A, , TSH np, Fe 17, UIBC 170, ferritin 295, PPD -

Hospital course: Headache and fever continued. Blood cultures were negative. On the 10 th hospital day the patient has a procedure performed and started treatment. This treatment produced a dramatic ending of her headaches and fever within 4 days. Later the IV urogram was normal.

Questions for Case # 7
1. What is the assessment for headache and fever?
2. What plan(procedure) was done on the 10 th hospital day?
3. What treatment was given which caused a dramatic ending of her chief complaints?
4. Why is fresh urinalysis needed?
5. What are causes of her abnormal urinalysis?
6. Does she have Fe deficiency anemia(IDA)? Explain your answer, please.
7. What is likely cause of her anemia?

Answers for Case # 7
1. Temporal arteritis/giant cell arteritis
2. Temporal artery biopsy, 3-4 cm. Report: giant cell arteritis/temproal arteritis
3. Prednisolone 30 mg/day.
4. Consider vasculitis with red cell casts which might dissolve on standing
5. Possible nephritis, or nephrosclerosis. Renal invlovement is rare in TA. The onset of hypertension in older age makes RA stenosis more likely, but less likely with neg Doppler.
6. No, increased ferritin suggests inflammation as acute phase reactant.
7. Anemia of chronic inflammation

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Case #6 12/17/97
27 year old man
cc: high fever and fatigue
HPI:10 days PTA onset fatigue and fever, no cold or other symptoms; 6 days before admission to clinic: ALT(GPT) 49, AST(GOT)65; day of admission con't fever, fatigue, ALT 786, AST 893. Medications: Qinolone and ampicillin and his wife's medication(unknown name) for 2 days. Social drinker[unknown amount] [ROS: no family members(wife and 3 yr old daughter) with any illness, no child care for daughter, no GI symptoms, blood transfusions, IV drug use, travel, change in diet, rash, arthritis or any other symptoms] [brackets indicate my own comments, no brackets indicates resident's comments]
PE: BT 38.5°, non-icteric, no liver tenderness, all np[nothing particular]
Lab: CRP 1.9, T bili .5> .8, ALP 460(<245), gGPT 223(<62), Chest x-p np, U/A 1+ protein, no cells; HAV IgM Ab (-), IgG (-), HbsAg (-), HBV Igm Ab (-), HCV Ab 2° (+), HCV Ab PCR 3° (-); all other routine studies np[nothing particular]

Hospital course: 12 th day no fever, LFT's near normal. [Bedside examination mild punch test for liver tenderness: no tenderness]

Questions for Case # 6
1. Is the liver dysfunction intra- or extra hepatic and why?
2. What type of hepatitis is most likely?
3. Describe type of immune complex disease?
4. Why is fresh urinalysis needed?
5. Should immune gamma globulin be used?
6. Should interferon be used?
7. What are indications for hepatitis patients to be hospitalized?

Answers for Case # 6
1. The liver hepato- cellular, dysfunction is intra hepatic because the bilirubin in normal. Intra hepatic obstruction is suggested by increased ALP & gGPT.
2. I suspect type C which can have acute presentation in 10% of HCV cases. The antibody tests for HAV and HBV are normal; HCV are + & -. That is my reason for suggesting HCV. But I am not sure about it. Drug induced hepatitis is also possible as a physician suggested.
3. Immune type hepatitis includes cases in young women and ANA +, and poly-arteritis nodosum(PAN) type with nephritis. These studies were normal.
4. Fresh urinalysis is needed to r/o nephritis with red cell casts. None seen.
5. Immune serum/ gamma globulin(IGG) should be used for close family contacts of HBV patients. Unknown benefit in HCV since transmission not clear[7/97 Arch Int Med article mentioned giving IGG decreased spread in sexual partners]. Not used.
6. Use of interferon for chronic HCV is for prevention of cirrhosis and carcinoma, unknown if benefit in acute HVC.
7. Hospitalization is indicated only if vomiting prevents fluid intake or hepatitis is fulminant. Perhaps this patient did not need hospitalization.

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Case #5 10/25/97
22 year old woman office worker
CC: Sore throat, fever and decreased appetite
HPI: 4 days before admission onset sore throat, 38 ° & decreased appetite
3 days before admission Local MD: 'tonsillitis' unknown treatment given.
day of admission to clinic, symptoms continue, onset dysphagia. Patient admitted
ROS(Review of Systems): 'kissing'
PE: 39.0°, 82 pulse, 120/60
Throat: bilateral white exudate over swollen tonsils
Neck: bilateral 5 mm tender anterior cervical lymph nodes
Chest: np
Heart: np
Abdomen: no liver/spleen

Lab: WBC 9, 900, 46% lymphocytes, 13% atypical lymphocytes, Hct 38, CRP 5.0,
AST/ALT 210/317, gamma GTP 186(n 37)
Abd ECHO: enlarged spleen
Anti EBV G and anti EBV M both increased

Tasks for Case # 5

1. Please complete your list of Assessment with differential diagnoses and etiologies, using the case archives tables as the format
2. Please complete your list of Plan with diagnostic studies and treatment, using case archives tables as the format

TABLE

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Case #4 9/3/97
21 year old male car driver with cc: acute severe dyspnea
HPI: One day before admission cough, sputum, sudden fever 37°, no sore throat, prior dyspnea, N/V; appetite,BM nothing particular(np). Admission day: continued feverish, acute onset chest discomfort while driving car at workcausing him to stop driving; he had tachypnea, dyspnea. He came himself to ER where pO2 was 42mmHg and he was admitted. S Hx: 20 pieces tobacco/d, occasional ETOH; F Hx np
PE 130/70 90, 38.4° RR 20 Alert with acute dyspnea Neck no JVD Chest clear Heart S1, S2, np, no S3/S4, systolic flow murmur 2/6 Abd, extremities, all np
Lab WBC 6,500, HmB 15.6, Plat 200,000, LFTs BUN,Creat BS Ca np, Na 134, K 3.3, CRP 4.6, ABG(ra) pH 7.57, pCO2 25.3, pO2 42, HCO3 23, Chest x-p np, ECG axis 75° IRBBB(no RVH or strain, S1 Q3T3), lung perfusion scint, chest C-T np, UCG 25 mm Hg PAP(?systolic), RA/RV np

Hospital course This distressing situation responded to simple nasal O2;intubation not required. I saw pt 5 days after admit: resting flat in not distress, systolic flow murmur heard.

Questions for Case # 4
1. What is your opinion about the correct diagnosis for this patient and give reasons supporting your diagnosis.?
2. What are his risk factors for PE?
3. What syndrome is suggested in patients with PE and no risk factors?
4. What treatments do you favor and why?
5. Solve the acid/base compensation equation.

Answers for Case # 4
1. There us no exact diagnosis for this patient. My opinion is PE is the most likely, perhaps 2° to antiphospholipid syndrome since usual risk factors are missing. Other remote Dx could be ARDS & AVM. Every patient with unexplained hypoxemia needs cardiac causes ruled out. Then every patient needs the calculation of the A-a O2 (alveolar-arterial oxygen) gradient. Using the standard formula: Start first to calculate the PA(alveolar) pressure : PA(alveolar) O2 = FiO2(Pb - P H2O) - PaCO2/RQ) = 0.21(713) - (40/0.8) = 149.73 - 50 = 100 in normal situations. But case # 4 had pCO2 = 25. Hence his PA O2 is 150-25/0.8 = 150- 31 = 119. So his A -a gradient is 119 - 42(his pa O2) = 77. Normal is 10-20 with older age adjustments not applicable to young person. Hence he has very great shunt. The most likely cause is PE, especially with his rapid improvement with simple nasal O2, and elevated PAP.
2. None, really. Car driving is not a know risk factor. That is why tests for antiphospholipid syndrome are needed.
3. see # 2 above
4. DIV heparin immediately until scintography and possible PAG has decided Dx. 5. Here is the formula: (change) HCO3 = 0.2 x (change) pCO2. = 0.2 x (40- 23) = 3.4. His HCO3 was 23, his change of HCO3 was 24- 23 = 1 as the actual change, and 3.4 as the expected change. Hence the HCO3 was higher than expected. Now it might be helpful to have the anion gap calculation to see if any metabolic acidosis is present. But the needed Cl- is not given. So we should assume that he had a mixed acid-base problem-the respiratory alkalosis dominates over the assumed metabolic alkalosis(actual HCO3 too high)

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Case #3 6/15/97
78 yo woman with edema of both lower extremities and R hand
HPI: 4 weeks edema of both lower extremities, not responding to Lasix 10 days before admission, R hand edema prompting visit to referral clinic and then admission No Review of Systems(ROS) PMH: DM for 15 yrs; Shx/Fx np Meds: sulfonylurea, glucosidase inhibitor, Lasix
PE 142/78, 36.3°, R24, BW 38Kg(prior 39) NP except for systolic murmur and 3+ pitting edema R hand, bilat. lower legs & feet
Lab:WBC 3,000, Hmb 8.1, Hct 25%, Plat 360,000, ESR 140, TP 9.1, Alb 3.0(Globulin 6.1), BUN 15, Creat 0.6, BS 225, U/A proteinuria neg x 3, Chest x-p np, ECG LAE, non-specific T wave changes. UCG mild increased PAP(35mmHg), small pericardial effusion, mild anterioseptal hypokinesis, slight increase RA RV LA, TR 2°, MR 1°.

Hospital Course: PE(bedside consultation):R wrist, MCP joints tender, decreased range of motion(ROM); bilat shoulders decreased ROM, bilat elbows synovitis, no nodules; L knee synovitis, pain on motion; bilat ankles pain on motion, , bilat. thigh muscle atrophy, Gr 1 systolic murmur, Gr 3 systolic/diasolic friction rub at L sternal border. After consultation a new diagnosis was made and she responded to new treatment.

Questions for Case # 3
1. What was the correct diagnosis for this patient?
2. What laboratory test might support the correct diagnosis?
3. What was the 'new' treatment?
4. Why was the correct diagnosis missed?
5. What was the cause of the friction rub?
6. Why was her Hmb and WBC decreased?

Answers for Case # 3
1. The correct diagnosis is rheumatoid arthritis(RA) supported by bedside findings of multiple symmetrical small joint tenderness and decreased ROM, and active synovitis shown by joint swelling. Differential diagnosis might include a polymyalgia rheumatica, and remitting seronegative synovitis of McCarty.
2. The supporting laboratory tests is the rheumatoid agglutination test: 3+
3. The new treatment was low dose prednisolone, 10mg/day.
4. The resident failed to ask the patient about pain and join pain specifically. The resident failed to perform a basic joint examination.
5. The pericardial friction rub represents the common asymptomatic chronic pericarditis seen in up to 50% of RA patients
6. The causes of anemia include chronic inflammation and Felty's syndrome of hypersplenism. Gastrointestinal bleeding needs consideration also.

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Case #2 2/20/97

25 year old woman office worker had chief complaint of high fever
HPI: 8 month before admission patient in excellent health, developed 38° fever, cough and sputum. Chest x-p showed 'pneumonia.' She was treated with antibiotics, temperature normal, no further follow-up. 3 weeks before admission 10 day trip to Hawaii during which she had increasing cough and sputum. When she returned home, she went to clinic and was admitted to referral hospital for high fever, shaking chills, cough, scant yellowish sputum. PMH/Shx/Fhx nothing particular(np), Review of Systems omitted
PE:120/80, HR 70, BT 40°, RR 25# alert, cyanotic lips, lungs right anterior, lateral and posterior crackles, +/- pedal edema, other sites np.
Lab(+only) WBC 9300, CRP 4.5, pH(ra) 7.49 pCO2 29, pO2 65, HCO3 22( respiratory alkalosis, hypoxemia), ECG sinus tachycardia, ? S1 O3T3, Chest x-p 2 masses, right upper and lower lobes with air-fluid level, diffuse patchy infiltrate right lower lobe, chest CT same.

Hospital Course: Patient was treated with 2nd generation cephem + clindomycin. Over next 6 days, fever down to 37.4°, pO2 normal, CRP 4/8, routine cultures np, chest x-p no change. One week later, smear showed AFB, patient sent to TB hospital.

Questions for Case # 2
1. How long has patient had active pulmonary Tb?
2. What errors occurred during the management of the illness 8 months before admission?
3. How long should it take to do Tb smear for AFB and get report?
4. What is usual work-up for pul embolism?
5. Is the patient immunosuppressed?
6. Were any of the airline passenger and hospital staff at risk for Tb?

Answers for case # 2
1. The duration of her Tb is unknown. It might have been present at the time of her first admission for pneumonia 8 months previously.
2. There was no follow-up chest x-p for the 'pneumonia.
3. Tb smear takes about 1-2 hours with immediate phone report when positive.
4. Pulmonary scintography is indicated for all patients suspected of pulmonary embolism. The value of D-dimer is not established. Cardiac ECHO is also not established. Heparin should be considered; PAG should be considered.
5. This patient was not clinically immunosuppressed. Her travels and sexual behavior may warrant HIV testing. Tb frequently occurs in immunocompetent people.
6. Yes airline passangers have been reported to develop + tuberculin skin tests after index case exposure; airliner air is recirculated. Medical hosptial staff are at risk to develop Tb if precaution are not taken. Hence all patient with Tb suspected require immediate isolation precautions.

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Case #1 12/10/96
49 year old woman CC Dyspnea
HPI: 96/1 dyspnea on exertion progressive to limiting walking to 10 meters. 6 days prior to admission, increasing cough> LMD> referral hospital and admitted. She had no orthopnea, edema, weight change. Fx, Sx np; no medications Review of Systems (ROS) not done
PE 120/90, R 18, P 90 Neck no JVD Heart increase S2, no murmurs Lungs and abdomen np Extremities ± cyanosis fingertips, no clubbing, no edema (Left 5-10 mm lymph node via neck ECHO)
Lab(+only) CBC, lytes, LFT, renal, np; D-dimer 4600(n10) Chest x-p: globular heart, CTR~ 51%, increased left hilar pulmonary artery ECG: NSR, ± increased P II,III, AVF, inverted T III, AVF room air pH 7.48, pCO2 27, pO2 57, HCO3 20(resp alkalosis) UCG: marked RA and RV dilation; valves(-), mild TR, PR, EF 69%, pericardial effusion 6-7 mm Abd ECHO: np Lung perfusion scan: multiple subsegmental defects Pulmonary angiogram: no specific obstruction of arteries, PA 82/42, mean 57, CAG np

Hospital Course: Patient was treated with standard doses DIV heparin. Patient died 3 days after admission. Autopsy(gross): signet cell gastric carcinoma, metastasis to lymph nodes; lungs: diffuse small tumors in small vessel and thrombi clots, liver(-), no gross vessel invasion. Consider Trousseau's syndrome-carcinogenic thrombophlebitis.

Questions for Case # 1
1. Is the patient's history adequate or accurate?
2. What is the value of Review of Systems(ROS) in this case?
3. Is the PE adequate or accurate?
4. What is assessment and plan from the abnormal ABG?
5. Is pericardiocentesis indicated?
6. Which clotting studies are needed?
7. Is the lymph node clinically significant?
8. What was accomplished by the 3 days of hospitalization?

Answers for case # 1
1. The history is incomplete. Questions to ask this patient include orthopnea, nocturnal dyspnea, chest pain, leg edema, sputum, blood in sputum.
2. ROS could have uncovered symptoms of gastric cancer including epigastric pain, dyspepsia, weight change.
3. The PE may be repeated after more data is obtained. The cardiac ECHO suggests markers of right heart failure. Hence a more careful search for JVD and TR would be helpful confirmation of right heart failure.
4. Using compensation equation change in pH/change in CO2 = 0.006 means partially compensated respiratory alkalosis.
5. The indication for pericardiocentesis is unclear. When the cause of the effusion is unknown the procedure should be considered. Cardiac tamponade, a clear indication, was not clinically present. However in this case, the assumption of PE as the cause is adequate since effusions occur in ~10% of cases of PE, and with the rapid down hill course, fluid analysis would not have changed the patient's outcome.
6. Other than using aPTT and PT for heparin and warfarin no other clotting studies are needed. DIC probably was not present since kidneys, skin, and CNS were not involved pre or post mortem.
7. The lymph node was not clinically significant pre-death since it was small and not palpable.
8. The 3 days of hospitalization culminating in death was horrific for patient and family, as well as hospital staff. The hospital support given family permitted the autopsy without which the cancer would not have been detected. Truth with compassion is better than speculation and possible fear.

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