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Ｃｏｎｆｅｒｅｎｃｅ ｉｎ Ｂｏｌｉｖｉａ, 1999
Conference in Bolivia, 1999
① Conference in Bolivia Feb 24thCase 52 yo M, married, farmerPresented by Dr. M.,
Past history； DM×2y. Pulm.TBC×1y(completed treatment for 8mo). Alcohol×17years.
Present il ness(summarized briefly)；8days ago, he started to have a precordial pain with diaphoresis. The pain lasted 17 hours. He was given a sublingual drug at an outside clinic and he was free of pain for two hours. He had taken drugs given, but stil had less intense pain. He came to EM of this hospital, but there was no bed available to him. He once went back home, but returned on the next morning and was admitted.
: How was the nature of pain? When did it occur? Night? Daytime? What was he doing then? How did it last for 17hr? Intermittently? Persistently in the same intensity? Did he eat and drink some or nothing while having pain?Dr. M.; He said the pain was oppressive and persistent in the same intensity. I didn’t inquire else.
Dr. Kurimoto; Myocardial ischemia does not give you such pain so long. But, there was accompanying diaphoresis. I cannot rely on what he mentioned.
Material of Past； EKG(taken at outside);low voltage in limb leads, q in AVFⅡⅢ, elevated ST in V2-6. Labs(EM);ALT10,LDH193,CPK110,GLU344,BUN41,CRN1.7,Na157,K3.7. WBC10000,Hb13,Hct41,ESR29.
Taken drugs;NTG10mg Isosorbide20mg Enalapril×4 times daily.
Dr. Kurimoto; Vitals at the time of coming to EM?Dr. M.; BP130/100, others not recorded
Physicals；There was no pain.
BP110/80 PR88R T36℃ Head and Neck;unremarkable. No jugular vein engorged. Lungs;crackles(BLL). Abd;unremarkable. Neurology;normal. No edema.
Dr. Kurimoto; What did you examine for neurology?Dr. M.; Muscle strength and sensory and gait and reflexes.
Dr. Kurimoto; Describe systematically. Motor system, muscle strength, muscle tone. Cordination and gait. Sensory system, light touch sensation,and likewise. ATR elicited?Dr. M.; Yes.
Dr. Kurimoto; I wonder. ATR is usually not elicited in elderly persons, since this longest nerve is easier to be degenerated than the others. This man is 52 yo, but diabetic. Proteinuria,if present,might be a sign of diabetic renal disease. Did you check cranial nerves?Dr. M.; Yes.
Dr. Kurimoto; How did you testⅠnerve?Dr. M.; I used my perfume.
Routine screening labs；Urine(P2+,S-,Keton-,SpGr1030,W2-3).
GLU270 CPK38 GOT18 LDH178.
Dr. M.; Urinalysis must be a Lab error.
Dr. Kurimoto; How much amount of urine was there in the bladder at entering hospital?Dr. M.; 150ml, for which urinalysis was done.
Dr. Kurimoto; Chest X-ray?Dr. M.; It was lost.
Dr. Kurimoto; Could you describe findings you took?Dr. M.; In bilateral lower fields there was hazziness with fine granules.
Dr. Kurimoto; Nothing else? No calcification or fibrosis?Dr. M.; No.
Dr.M. #1 acute myocardial infarct #2 diabetes mel itus
Dr.C. #1 precordial pain→acute myocardial infarct→congestive heart failure #2 hyperglycemia #3 congestive heart failureDr. P. #1 acute myocardial infarct #2 diabetes mel itus #3 cardiomegaly #4 proteinuria #5 hypernatremia #6 alcoholism
Dr. Kurimoto; Which is the preceding,AMI or DM? What number would you give to a supposed grave disease that occurs tonight? The preceeding is #1 and the latest is # the highest. Dr. C., how did you treat your #3 on your list? Eliminated and moved to #1? If so, what happened to AMI on the list? Was AMI lost somewhere?
Dr. Kurimoto #a hyperglycemia #b proteinuria #c acute myocardial infarct #d congestive heart failure(#c)
Dr. Kurimoto; The data base is not sufficient. Dr. M. suspected a Lab error on urinalysis. I am sorry I could not rely on his physicals especially of neurology and of chest X-ray findings. In a case of positive ATR, I almost exclude diabetic peripheral neuropathy, which should be seriously considered in this case. I also wonder how to think of tuberculosis which is said had been treated fully. But there was no residuum on the film. Therefore, my list is temporary for the time being. The cause of #d is depicted by a parenthesis.
Dr. P.; Why don’t you put hypernatremia and alcoholism on the list? Alcoholism can cause pancreatitis or liver cirrhosis.
Dr. Kurimoto; Hypernatremia is a sign of transient dehydration which must have been brought about by probable decrease in oral intake. It will disappear on proper hydration. Pancreatitis or LC is not a part of alcoholism. It is another disease,although alcohol can be etiology. What do you include in alcoholism? Dr. P.; No stop drinking alcohol.
Dr. Kurimoto; It is a mental part of alcoholism. There should be a physical part of alcoholism. Even if you cannnot stop eating “carne”, you wouldn’t call it “carneism”.
② Conference in Bolivia Feb 26thCase 76yo M, Rancheon ownerPresented by Dr. C.,
Present il ness(summarized briefly)；A month ago he started to have shoulder pain for which NSAID was given. 20 days ago he had hematoemesis and melena, and an endoscopic diagnosis of an ulcer at gastroesophageal junction was made. On the day of coming he had hematochezia 2-3 times a day and 1 time in a large amount.
Past history； diverticulosis 4years ago.
Dr. Kurimoto; What was the patient doing then? The hematochezia sudden? Didn’t he have pain, fever or nausea at all? Could he walk alone right after he bled?Dr. C.; I don’t know what he was doing, but it was sudden without any other symptoms. He walked and came on foot.
Dr. Kurimoto; He didn’t collapse, that suggests an amount of blood suddenly lost then was not so large a
s to bring hypovolemia.
Physicals；Pale skin, dental caries. BP140/70 PR58R RR12. Heart apex; 5ics on MCD no mm. Lungs;clear. Abd;bowel sound normal, otherwise unremarkable. rt-Elbow; ankylosed. Bilateral shoulder; range of motion limited.
Dr. Kurimoto; Do you properly use your stethoscope? First apply a bell for low-pitched sounds,then a membrane for high-pitched. Are you sure ofneurology?
Screening routine labs；Urinalysis;P-S- .Hb11.2 Hct 35 W10100 Plt775000. Na149K5.2 GLU98BUN36(n) CRN1.1.
Hospital course；He bled for 3days,3-4times a day. And then bleeding stopped. Colonoscopy reports 1diverticulitis, 2angiodysplasia in caecum and descending colon, 3 a 2×1.5cm tumor in anal canal which was biopsied to show vil ous adenoma. He
had received 3000ml of transfusion and Hb is now 12.4.
Dr. Kurimoto; Was there no blood in the lumen of bowel on colonoscopy?Dr. C.; No.
Dr. Kurimoto; Diverticulitis is a diagnosis. Describe the findings first. Site? One at the free wall can give rise to perforation. How many? How did youknow it was diverticulitis? What findings? Edema? Hyperemia?Hemorrhage? Dr. C.; Nothing is mentioned.
Dr. Kurimoto; No hemorrhage on the surface of the adenoma?Dr. C.; No.
Dr. Kurimoto; Any lesion at gastroesophageal junction?Dr. C.; None.
Dr.C. #1diverticulitis #2arthrosis #3upperGI hemorrhage
Dr. M. #1lowerGI hemorrhage #2diverticulosis #3anemia(#1)
Dr. Kurimoto #1 arthrosis(used“Spanish”term) #2 lowerGI hemorrhage(#3)
#3 colonic angiodysplasia #4 vil ous adenoma #a diverticulosis
Dr.Kurimoto; MCV, MCH were not mentioned. If they show microcytic and hypochromic,what is suggested? And what is suggested by thrombocytosis (Plt775,000)?Dr. C.; Bleeding is chronic.
Dr. Kurimoto; Yes,may be Fe deficient RBC. This is reactive thrombocytosis,which occurs in acute bleeding or active inflammatory diseases.
Dr. P.; Thrombocytosis is characteristic for Crohn’s disease.
Dr.Kurimoto; We’d better to think that Crohn’s disease is one of active chronic inflammatory diseases, so that it is accompanied by reactive thrombocytosis. In any chronic active inflammatory diseases,you could expect thrombocytosis.
Does normal BUN suggest you something? Blood had not stayed long in the intestine. So, it is an indirect evidence of no upperGI bleeding. A suddenbleeding with no preceeding and accompanying symptoms is characteristic of vascular and neoplastic source. If the villous adenoma were the source, I would expect mucosal or submucosal recent hemorrhage on its surface.
I believe the source is angiodysplasia. I am reluctant about the diverticular
disease, since no good description of findings was obtained.
What is the commonest underlying disease of colonic angiodysplasia in elderly persons? Well, aortic stenosis is common. Didn’t you have a murmur of that valvular disease?Dr. C.; I think not.
Dr. Kurimoto; Let’s go and see the patient.
Dr. P.; Are skin pigmented spots and the ankylosed elbow not problems?Dr. Kuimoto; No. They are simply physical findings of this patient.
③ Conference in Bolivia Mar 5thCase 31yo F, housekeeper, born in Val egrande Presented by Dr. M.,
Present il ness(summarized briefly)；On Feb 14th, 2 hours before she entered the hospital, she suddenly became unconscious. After 1 hour she recovered and vomited green liquid with food stuff. She noticed her right arm and leg weak and also dysarthria. She felt dizzy, and palpitation and dyspnea especial y at night.
Past history；Left arm burnt,3 year oldIschemic vascular accident of brain(left side),2years agoMitral stenosis detected 2 years ago(warfarin taken for 3 months)
Materials of past；Head-CT(1997); a large low dense lesion almost occupying a whole left hemisphere of cerebellum
Dr. Kurimoto；What was she doing, when she lost consciousness? Was not there convulsion or incontinence? Is this the first and no similar episode before?Dr. M.；She was angry and argued about a family problem. There was neither convulsion nor incontinence. She had a similar loss of consciousness 2 years ago.
Dr. Kurimoto；You have to write these in the note. Only what is written is a record.
Is it clear to you the difference between dyspnea and shortness of breath? What would you get on running fast or going up on a steep slope of La Paz?
Dr. M.; Dyspnea.
Dr. Kurimoto; Explain Dyspnea.
Dr. M.; A subjective feeling of need of air.
Dr. Kurimoto; Dyspnea is a distress of each breathing, inspiratory or expiratory or both. Shortness of breath is simply a feeling of tachypnea with no distress of each breathing which is smooth and easy. The mechanism is different. We shall have shortness of breath at La Paz.
No arhythmia recorded 2 years ago? Did the palpitation come and go suddenly? Or gradually?Dr. M.；No arhythmia recorded. Palpitation was gradual.
Dr. Kurimoto; Dysarthria is a tem of judgement. Replace it by a term of fact. What sound could not she make well? Lip? Tongue? Throat? This may be a part of physicals,though. Make sure of dizziness or vertigo.
Dr. M.；Lip sound.
Physicals；She could not stand and walk. Glasgow scale 13/15. BP120/70 PR105R RR20. Head and neck; eyes deviated to right, pupils round and respond to light, tonsils congested, no lymphnodes, thyroid non-palpable. Heart; apex 6ics and 1cm lateral to MCL,S1 accentuated and S2 less intense, diastolic murmur at 5ics on MCL. Lungs; clear. Abd; soft and non-tender, no organs palpable, bowel sound normal. Extremities;hypotonic and muscle strength weak on both sides, more on the left, sensory for pain decreased on the left(since 2 years ago), al DTRs hypoactive more on the left.
She recovered from the right hemiparesis in 3 days and now walks with assistance.
Dr. Kurimoto; You must describe about a murmur maximal point, phase, duration, intensity and pitch.
Dr. M.; It is a pan-diastolic and high-pitched and audible only on that point.
Dr. Kurimoto; Not radiated to anywhere else?Dr. C.; Only mitral area. Dr. Kurimoto; What is mitral area?Dr. C.; 5 th intercostal space on slightly lateral to midclavicular line.
Dr. Kurimoto; Do not use a fixed word as mitral area. Jet stream through the
mitral orifice goes to the apex. A thin vertical heart gives you the mitral sound to the lower front of the chest and an enlarged horizontal heart to the very lateral even to the back. No fixed site. Your description of the murmur only audible medial to the apex seems to suggest aortic regurgitation. But, I can hardly imagine of pan-diastolic murmur.How did you test pain sensation? Dr. M.; I pinched the skin
You described only a part of cranial nerve functions.
Labs；Urinalysis;lost. BUN26 CRN0.8 Na142 K4.3 GLU11. PT80%. W10600 Hb 11.2 Hct 35. ESR40 ASO 333 CRP4.8. EKG; sinus rhythm, enlarged left atrium.
Chest X-ray(AP); heart enlarged, pulmonary arteries and left auricle enlarged,pulmonary congestion.
UCG; severe mitral stenosis, good systolic contraction.
H-CT; a large low dense area in the left cerebel um, cerebral edema.
Dr. Kurimoto; ASO is unnecessary. The rheumatic disease is fairly remote. This EKG shows, to me, slight right axis deviation, biphasic wide P at V1-2, RS pattern at V1-6, negative T at V1-4. Now, what is your EKG diagnoses on these findings? My EKG diagnoses are left atrial hypertrophy and probable right ventricular hypertrophy. On Head-CT, you must have thought of edema because of much low dense feature of the white matter contrasted with the gray matter. But, you can see clear sulci of cortex, no distortion of the ventricles and symmetry of the structures. This is not cerebral edema. This feature is called periventricular lucency and there may be lacunar infarcts.
Does the UCG report mention the orifice area, EF and so?Dr. M.;
Dr. M. #1 mitral stenosis #2 TIA #3 cerebel ar syndrome
Dr. C. #1 mitral stenosis #2 TIA
Dr. Kurimoto #1 mitral stenosis #2 cerebel ar infarct #3 TIA
Dr. Kurimoto; What is cerebellar syndrome?
Dr. M.; cerebellar motor dysfunction.
Dr. Kurimoto; I don’t see it here.
Dr. M.; There is intention tremor.
Dr. Kurimoto; Dr.M. did not mention that on the data base, did he? Dr. C.; No.
Dr. Kurimoto; We all don’t know about it, because the data base we were given lacks that information. That should have been present in the data base. Then, we share all of the information to discuss effectively and can learn each other. We are all students of medicine.
Dr. C.; Cerebellar dysfunction is not on your list. There would be an infarct but without dysfuction. Isn’t it better to list it up?Dr. Kurimoto; I think that a problem:cerebellar infarct includes cerebellar ataxia. In absence of ataxia, an infarct would be very small, I shall regard it one of radiological findings and not a problem. Shall we go and see the patient and try to obtain a complete cardiology and neurology?
④ Conference in Bolivia Mar 10 thCase 23 yo F student of nurseryPresented by Dr. C.,
Present il ness(summarized briefly)；5 years ago, she noticed her right eye to be deviated first to right side and, then to left side. She lost the vision of the right eye. There was retrobulbar pain. In a month her symptoms gradual y and total y disappeared. 4 years ago the same symptoms occurred on the left side. Again she recovered completely. 3 years ago she was asthenic in lower extremities, and had left side paresthesia and intentions tremor. Gait was difficult. In 5 months she could not walk without assistance and recently became unable to stand. Past and family history； none.
Material of past； none.
Physicals；Pupils;isocoric and light reaction normal. Nystagmus; toward right on lateral gaze to right. Heart and lungs and abd;unremarkable. DTR ｓ al hyperactive. Babinski positive on both sides. Muscle strength 5/5. Vision; decreased in left
side, field normal.
Gait ;wide-based, tandem unable. Romberg positive. Finger and toes;dysmetric. Sensation; normal for light touch, pain and temperature.
Dr. Kurimoto; You’d better to present neurology systematically. In motor system, how was muscle tone and in sensory system, deep joint sensation? Dr. C.; I didn’t check.
Dr. Kurimoto; You mentioned only pupils and nystagmus about the cranial nerve functions. How were the others? Dr. C.; normal.
Dr. Kurimoto; You must write them in the note.
Dr. C.; I didn’t write,because they were negative. Dr. Kurimoto; You have to. Deep joint sensation cannnot be said negative, which you didn’t check. Unless you write, nobody can know it’s negative. You know about Dr.Burkitt who discovered Burkitt lymphoma in Africa. Many years ago, he came to USA and addressed a meeting. He showed us a photo-slide of a beautiful clinical description of a child found in an old record, which was just the same as of the children he was seeing. You write and you are sending a message to the future years of hundreds.
Laboratories；Hb12.1 Hct 38 W5400 Plt 280,000 ERS27. Urinalysis;P-S-W2+R2. GLU90 Bun14 CRN0.7 Na140 K4.2. Chest X-rays;the patient took it away. EEG;normal. Head-CT;normal,no atrophy. Auditory brainstem; evoked response decreased in both,more in right.
Dr. C. #1multiple sclerosis #2cerebel ar syndrome(#1)
Dr. Kurimoto; How did you reach a diagnosis of multiple sclerosis? Dr. C.; The neurologist said this is typical.
Dr. Kurimoto; You simply took his word, didn’t you? Suppose you had been in charge of the patient since 5 years ago, what would be your initial problem list?Dr. C.; #1optic neuritis.
Dr. Kurimoto; How come optic neuritis?
Dr. C.; An ophtalmologist diagnosed.
Dr. Kurimoto;Then, you renewed the problem list; #1optic neuritis→multiple sclerosis #2cerebellar syndrome. Optic “neuropathy” might be a better term,though.
Dr. C.; Yes.
Dr. Kurimoto; Is #2 transferred to #1 or still present? Dr. C.; Still present.
Dr. Kurimoto; Etiology of #2 was determined as #1. So, the following would be the way you took in considering; #1optic neuritis→multiple sclerosis #2cerebellar syndrome(#1).
Dr. C.; Yes.
Dr. Kurimoto; Then, show us your analysis of #1 to arrive at a dx of multiple sclerosis, namely differentials.
Dr.C.; Remission and relapse of the disease in a young woman is characteristic of multiple sclerosis.
Dr. Kurimoto; You mentioned only a clinical course of disease.There are other diseases which show remission and relapse in young people.
Dr. La F.; Anatomical analysis is necessary.
Dr. Kurimoto; Exactly. Analysis, please. How did you exclude the other diagnoses?Dr. C.; I don’t understand how to analyze.
Dr. Kurimoto; Let’s check each finding. The nystagumus indicates a vestibular system lesion. Is unilateral decreased vision an optic nerve disease in this patient? Did you have an ophthalmoscopic finding? Could be a retinal disease? Lower motor unit is saved,but the upper is diseased manifested by hyperactive DTRs and Babinski. Ataxia here is a sign of cerebellar lesion, although we are not aware if posterior column lesion is present. Spinothalmic system seems to be saved. Are these dysfunction present in this young woman caused by a solitary lesion of one location? Dr. C.; No. The lesion is diffuse.
Dr. Kurimoto; The lesion is not diffuse and symmetrical. Better to say the lesions are multifocal. Unilateral optic neuropathy and an unilateral vestibular disease without overt hearing troubles can be mononeuropathy multiplex, but the cerebellar disease is not. This is a multifocal disease scattered randomly but throughout in central nervous tissue, foci being small evidenced by a normal H-CT. What can cause this type of lesion? Vasculitides, granulomas
possible, of course a demyelinative disease is possible. Remember the disease is chronic and can remit and relapse,and also it occurred in such a young girl. No lesions are present outside the nervous tissue. Vasculitides or granulomas are unlikely. Of which problem is this to be written in A? What evidence is against multiple sclerosis?Dr. C.; Not elevated ESR.
Dr. Kurimoto; I agree. I expect worse ESR in active multiple sclerosis.
Dr. C.; May be the disease is in remission.
Dr. Kurimoto; No. The history suggests the disease has been now active and progressive.
Mr. M.(Laboratory); What is the normal in this lab? How was ESR in other diseases?Dr. C.; In one case of active SLE and in tuberculosis, it was more than 100.
(Mr. M.; personal communication; In this lab the normal ESR is lower than in the other labs,because the blood sample is of a half amount and the reagent is EDTA instead of citrate
.) Dr. Kurimoto; What would be your diagnostic plans for #1? Dr. C.; Ophthalmoscopic study.
Dr. Kurimoto; It already gave you a diagnosis of optic neuropathy. No need more. #1 optic neuritisA ： Cerebrospinal fluid analysis is necessary to conform multiple sclerosis strongly suggested by the data base.
⑤ Conference in Bolivia Mar 12Case 22 yo F homeworkerPresented by Dr. M.
Present il ness(summarized briefly)；1 month ago, she started to have cough and sputa, which was white to yel ow. There were fever,asthenia, anorexia and night sweat. She lost 4kg ofbodyweight in a month. She was started anti-tuberculosis regimen(INH,RFP,SM,PZA),since acid-fast bacili were found in the sputa on two occasions. 10-15 min after the first administration of the drugs, pruritic rash appeared al over the body and lip edema and dysphasia as wel . She vomited
but had no abdominal pain or diarrhea. The rash was disappearing in 24 hours, but stil persisted and she came to the hospital.
Family history and past history；2 years ago; pulmonary tuberculosis (INH,RFP,SM,PZA given for 8 months)
Dr. E.; How were all of the four drugs given? At once?Dr. M.; Yes.
Dr. Kurimoto; No blood in the sputa? Dr. M.; No.
Dr. Kurimoto; The drug history was told by the patient? When you mention in the history, it indicates that the patient told. Otherwise, it should be inmaterials of the past.
Dr. M.; She knows and told.
Materials of past；A rural hospital; (2 years ago); She was treated for pulmonary tuberculosis and recovered wel by INH,RFP,SM,PZA given for 8 months. (this time); Sputa bacteriology positive for acid-fast bacili on two occasions.
INH,RFP,SM,PZA given once.
Chest X-ray: RUL high density and diffuse macronodules.
Dr. Kurimoto; Please tell us your findings on the chest x-ray film, Dr. C.?Dr.C.; A cavity in RUL. Space between right upper ribs is narrowed to indicate RUL volume decrease. Dr. Kurimoto; Don’t go first to your point of interest. Start from a general survey. I see no fat line in the soft tissue of the chest wall, which must have been exhausted. Right hemidiaphragm is elevated by one intercostal space, normally at 10th ics in the posterior aspect. This indicates the right lung volume decrease. Adding to Dr.C., elevation of right hilum and, here you see, trachea deviation to right indicate RUL volume loss. Compensatory hyperinflation of the other lobes is suggested, you see, by widening of the space between the lower ribs. There are scattered micronodules maximally measuring 0.2cm with linear densities. I don’t know your terminology, but I don’t say macronodules. RUL is consolidated and loses some volume, in which I see three cavities, maximal one being 4cm. The margins are smooth and
they contain nothing. Calcification is absent. Chest x-ray diagnosis is cavitary pulmonary tuberculosis of right upper lobe. Micronodules may be collections of inflammatory infiltrates or granulomas. I don’t know which.
Physicals; Cachectic. Pale and wet. BP80/40 PR 118 T37.7℃ Diffuse papules. Pharinx congested. No lymphnodes and thyroid palpable. Chest; symmetrical, expansion decreased on right, RUL and RML subdull on percussion, right apex and RML crecitpitatio on auscultation. Heart; apex 5ics on MCL,unremarlkable. Abd; soft and flat, no organs palpable, bowel sound normal. Ext;diffuse muscular atrophy,strength 5/5. DTRs normoactive. Coordination and sensory unremarkable.
Dr. Kurimoto; Did you see rash in the palms, too? Did you check dermography?Dr. M.; Palms were pruritic. No, I didn’t check it.
Dr. Kurimoto; Lung-liver border?Dr. M.; 6ics.
Dr. Kurimoto; Unless you really examine,don’t make a guess. Did the liver move on respiration? Which segment of the lungs did you notice dullness and crecipitatio?Dr. M.; I don’t know.
Dr. Kurimotro; The other day on bedside, I showed how to check every lobes on physicals. The heart sound is said normal. In cases of chronic pulmonary disease, the pulmonic part of S2 is not uncommonly accentuated by pulmonary hypertension.
Laboratories；Hb10.8 Hct34 Plt370,000 W8100 (b1 seg86 Eo7 Ly6 Mo 0) ESR 31(n-10) Urinalysis;P and S not reported W2-3 R100 GLU93 TP7.9 Alb4.7 Sputa;acid fast bacil i positive on two occasions.
Dr. Kurimoto; Did you inquire of the lab a kind of the cells in the sputa?Dr. M.; No.
Dr. Kurimoto; If you see many neutrophils in TBC, there are two possibilities, one being a complicated bacterial disease and the other being an acute TBC
disease. Was not she in menstruation at urinalysis? When was the last period? Is she not amenorrheic? Dr. M.; I didn’t inquire.
Dr. C.; I will go and inquire. (Returned)She has been on menses from Mar 5 th to 10 th.
Dr. Kurimoto; She was on menses. Urine RBC is contamination.
Hospital course；Anti-TBC drugs have been tried each by each, started from INH and RFP,SM. The rash has not worsend so far. PZA is not tried yet.
Dr. M. #1pulmonary tuberculosis #2drug al ergy #3anemia
Dr. Kurimoto; Let’s think about #2. Drug allergy includes many different diseases, anaphylactic bronchospasm, drug-induced hepatitis, urticaria and so. It can be comparable with stapylococcal infection in a sence, that includes many different diseases from meningitis to a tiny skin abscess. Clinical disease entirely differs. Now, you understand that drug allergy and staph.infection indicate a nature of diseases and,drug and staph.are etiology of the diseases. They are not a name of problem. List up a problem.
Dr. La F.; Dermal papule.
Dr. C.; I don’t know. Please show yours.
Dr. Kurimoto; I would say diffuse pruritic erythopapular dermatopathy. Drug is strongly suspected and your plans were right, I think. But until the etiology is confirmed, I don’t put Drug-induced to the problem. Suppose PZA does not aggravate the rash, how would you interpret?Dr.E.; Some other intoxication. Many times etiology cannnot be determined. Dr. P.; Etiology still is not evident. Drug disease is in strong suspicion. Would you stop giving the drugs? Dr. Kurimoto; No. All of the drugs cannot be etiology. Fortunately, this patient’s probable allergy is a dermal disease. Bronchus or intestine is spared, which can threaten a life. In a case of such grave diseases, I would try each drug in preparation of immediate administration of catecholamines and steroids. We have an elevated ESR. What substance causes to elevate ESR?
Dr. C.; I don’ｔ know.
Dr. Kurimoto;Globulin and fibrinogen cause elevation of ESR. But you have here normal albumin-globulin ratio. Hypergammaglobulinemia is expected in chronic active inflammation. This is not a very acute disease in which hyperfibrinogenemia occurs. The serum protein result is a bit difficult to interpret for me. #3anemia and #4malnutrition are not on my problem list. Hb10.8 is in the range of active TBC. Serum albumin was 4.7. Can it be protein-energy malnutrition? And she is not amenorrheic.
Dr. C.; Is not lymphocytopenia a problem? This is a second disease of TBC. Immunoinsufficiency should be suspected. Dr. Kurimoto; May be. I would go down to the lab and see the smear by myself. Until then, I don’t put it as a formal problem.
Dr. La F.; How about PPD?Dr. Kurimoto; It’s a good suggestion. PPD is a simple way to evaluate immunocompetence.
Dr. C.; Hematuria is another problem.
Dr. Kurimoto; Don’t you believe contamination of menses?Dr. C.; Another disease is possible.
Dr. Kurimoto; I believe it’s from menses.
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