Hofmeyr, N. G.

Retief, F.P.

English

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96 S.A. MEDICAL JOURNAL 30 January 1965ACUTE HAEMOLYTIC ANAEMIA AS A COMPLICATION OF TYPHOID FEVERF. P. RETIEF, M.B., CH.B. (CAPE ToWN), D.PHlL. (aXON), M.R.C.P. (EDIN.) AND N. G. HOFMEYR, M.B., CH.B.(CAPE TOWN), From the Department of Internal Medicine, Karl Bremer Hospital, Bellville, CapeHaemolytic anaemia as a rare complication of typhoidfever was first recognized by OsIer in 1895.1 Since then,however, less than 40 authentic cases have been describedin the medical literature.l.16.20 We wish to report a patientwho had typhoid fever and presented with acute intravas-cular haemolysis.CASE REPORTA 36-year-old Bantu labourer was admitted to the Karl BremerHospital on 11 March 1963. He had been in good health until3 days previously when he fainted on arriving home fromwork. He subsequently passed much red blood per rectum andfelt weak and feverish. The next day he remained in bed withprogressive malaise and headache and noticed that his urinehad become 'like black coffee'. At no time did he experiencerigors, vomiting, diarrhoea or significant abdominal pain. Onthe third day of his illness he again passed blood per rectumand was admitted to hospital.The patient had come from the Transkei a year previously.His past history and further clinical interrogation revealednothing else of note, except 'kidney trouble' in 1954_ Notyphoid contacts could be traced.Clinical ExaminationAn ill, well orientated man of normal build presented witha temperature of lOZOF and a respiration of 24/min. Therewas mild scleral jaundice but no significant adenopathy,bleeding tendency, splinter haemorrhages or skin rashes.Cardiovascular system. BP 150/90, pulse 84/min. (goodvolume), heart normal.Abdomen. Mild peri-umbilical tenderness but no masses orperitoneal irritation; liver was just palpable but spleen notclinically enlarged; rectal examination showed melaena butno other abnormality; proctoscopy was norma!. The rest of(he clinical examination was non-contributory.Urine. Dark red colour. Microscopy: abundant epithelialcells but no red cells, pus cells or cylinders. Chemical tests:protein + + +; orange sugar reduction with Benedict's re-agent; bile and urobilinogen not demonstrated; porphyrinsabsent. Spectroscopy: oxyhaemoglobin present.Peripheral blood. Hb. 5·8 G /100 ml.; PCV 16%; MCHC36%; leukocyte count 30,OOO/cu.mm. (Iymphocytes 14%, neu-trophils 77%, staff cells 4%, metamyelocytes 5%, occasionalmyelocytes); normoblasts 4/100 leukocytes; reticulocyte count54%; platelets 289,OOO/cu.mm.; ESR 40 mm./lst hour. Wester-gren. Red cell morphology showed severe anisocytosis, largenumbers of spherocytes, 'triangular cells' and fragmentedmicrocytes.Special Investigations1. Haematology. (11 March 1963) Serum spectroscopyshowed oxyhaemoglobin bands but no methaemoglobin, sul-phaemoglobin or carboxyhaemoglobin. Schumm's test wasnegative. (12 March) L.E. cell investigation negative. Heinzbody preparation negative. Direct and indirect Coombs' testswere negative at 3rc and 2ZOC. Bone-marrow aspirationshowed hyperactive normoblastic erythropoiesis and hyper-active myelopoiesis.2. Blood biochemistry. (12 March) Blood urea was 16 mg./100 ml. Serum proteins: Albumin 4·5 G/lOO m!., Globulin 3·2G/lOO ml. (increased a 1, /3 and S globulin). Bilirubin 2·7 mg./lOO m1. (direct 0·5 mg./lOO ml., indirect 2·2 mg.f100 ml.);direct Van den Berg reaction negative. Transaminase (SGPT)64 Cabaud units/ml. Alkaline phosphatase 2·4 Bodansky units/lOO ml. Thymol turbidity 2 units, thymol f1occulation 0 unitand zinc turbidity 4 units. Cholesterol III mg./l00 m1. (15March) Fasting blood sugar 152 mg./l00 ml.3. Ellood Wassermann & VDRL tests were negative.4. Agglutination tests (12 March) Widal negative, Brucellanegative, Weil-Felix negative, Paul-Bunnell negative.5. Blood cultures. Salmonella typhi were isolated on March11, 12 and 14, but on 15 March no growth could be obtained.Progress and TreatmentThe clinical picture was that of acute intravascular haemo-lysis. In the absence of a satisfactory diagnosis, no specifictherapy was instituted except for a blood transfusion of 4pints. The patient appeared remarkably well in spite of signi-ficant pyrexia (99·5°F - 105SF) and a rising blood urea-45 mg./lOO ml. (13 March); 64 mg./l00 ml. (15 March); 104mg./l00 ml. (16 March). However the urine output remainedsatisfactory and on 26 March the blood urea had fallen to48 mg. /I00 ml.The haemoglobinuria decreased rapidly and disappeared onthe third day after admission. All clinical signs of haemolysiscleared in the course of a week, and the haemoglobinstabilized at 11 G /100 ml.On the 5th day after admission severe rectal haemorrhagerecurred, necessitating a blood transfusion of 8 pints. On thesame day the Microbiology Department reported isolation ofSalmonella typhi from blood cultures taken on admission.Immediate treatment with chloromycetin (500 mg. 4-hourlyfor 3 days followed by 500 mg. 6-hourly) was instituted and 5days later the patient was apyrexial.The glycosuria and raised blood sugar values suggested dia-betes mellitus. On a 1,200-calorie diabetic diet the glycosuriadisappeared and the blood sugar fell to 74 mg. /100 m!. (26March).No further complications were noted and on 27 March hewas transferred to the City Hospital for Infectious Diseases,where he made an uninterrupted recovery.Subsequent follow-up was not possible as the patientreturned to the Transkei after discharge from hospital.DISCUSSIONThe occurrence of haemolytic disease in the course oftyphoid fever might not be as rare as is generally thought.Osler1 found I case among 1,500 typhoid patients, butHuckstep20 in 1962 recorded an incidence of 2%, whileBerman et af.l2 found an incidence of 5·9% in 1945.McFadzean and Choa14 reported the rather similar figureof 4·6% among the Chinese of Hong Kong in 1953; theyremarked on the absence of haemolysis in paratyphoid A,Band C. Nevertheless Ruggieri16 as recently as 1961reviewed the world literature and could find no more than32 reported cases of haemolytic anaemia from salmonellainfections, and at least 5 of these are doubtful instances.4.'The mechanism of haemolysis is not clear. As happenedin our case, at least 50% of the reported instances of acutetyphoid haemolysis with haemoglobinuria occurred duringthe first week of illness, when bacteraemia is known to bemaximal. However, me salmonella is normally an anhae-molytic organism. Although early work by Friedbergerand Vallen17 in 1923 did suggest that bacteriophage inter-action may render the salmonella haemolytic under certainexperimental conditions, this is unlikely as a spontaneousoccurrence. McFadzean and Choa14 noticed that haemoly-sis did not parallel me severity of infection but outlastedthe pyrexial illness. A large proportion of their cases alsohad a positive Coombs' test and seemed to respond toACfH rather man to antibiotics. They therefore sug-30 Januarie 1965 S.A. TYDSKRIF VIR GENEESKUNDE 97gested an underlying auto-immune aetiology, possiblyassociated with the lymphoid hyperplasia of typhoid fever.Our patient was Coombs-negative and the haemolyticcrisis cleared after a blood transfusion in the presence ofundiminished pyrexia. Rapid disappearance of clinicalhaemolysis as well as repeated large blood transfusions,necessitated by recurrent intestinal haemorrhage, hinderedsatisfactory appraisal of the haemolytic process. However,the investigations performed showed no cause for haemoly-sis besides the obvious systemic infection. Heinz bodiessuggestive of 'drug-induced' haemolysis were not demon-strated, but the glucose-6PO4 -dehydrogenase content of hiserythrocytes was not estimated. McFadzean and Choa14considered ACfH of great therapeutic value in their cases,but Ruggieri16 reported a disappointing response to predni-sone. Nevertheless, one feels that steroid therapy should beinstituted in this condition, as its value is well establishedin fulminating typhoid.18The present case illustrates the protean manifestations ofatypical typhoid fever. In addition to the haemolyticepisode the patient presented with severe intestinal hae-morrhage during the first week of illness. The persistentleucocytosis and tachycardia can be partially attributed tothe acute blood loss and haemolytic reaction. DiabetesmeIlitus is not a recognized complication of typhoid, butlatent diabetes may be unmasked by the stress of anysevere systemic illness.19AbstractSUMMARYA case of typhoid fever is reported, which presented with acuteintravascular haemolysis and melaena during the first week ofillness. The literature on typhoid haemolysis is briefly reviewed;the association is possibly less uncommon than is generallythought.We wish to thank Prof. A. J. Brink, Department of InternalMedicine, Stellenbosch University, for his stimulating interest,and Dr. R. L. M. Kotze, Medical Superintendent of KarlBremer Hospital, for permission to publish clinical material.REFERENCESI. OsIer, W. (1895): Johns Hopk. Hosp. Rep., 5, 311.2. Curschmann, H. (1898): Specielte Pathologie U. Therapie, (Vienna), 3,177.3. Musser, J. H. and Kelly, A. O. (1901): Phi!. Med. J., 7, 119.4. Mouisset, F., Monguand, G. and Thevenot, L. (1906): J. Physiol.Path. gen., 8. 508.5. Sicard, J. A. and Guttman, R. A. (19U): Bull. Soc. med. Hop. Paris,33, 10.6. Marcora, F. (1919): Policlinico, Sez. med., 26, 424.7. Stanzoni, M. (1924): Rif. med., 40, 1063.8. Kadmka, S. (1928): Sang, 3, 536.9. Flaudin, C., Bernard, J. and Mallarme. J. (1935): Op cit."10. Castellanos, A. and Montero, R. (1940): Arch. Med. interna (Parma),6. 232.11. Wright, F. J. (1945): E. Mr. Med. J., 22, 24.12. Berman, S. E., Brann, K. and Rachmilewitz, M. (1945): Acta med.orient. (Tel-Aviv), 4, 175.13. Shaw, A. B. (1951): Lancet, 2, 813.14. McFadzean, A. J. S. and Choa, G. H. (1953): Brit. Med. J., 2, 360.15. Smith, C. E. G. (1951): Lancet, 2, 1020.16. Ruggieri, p. A. (1961): Delaware Med. J .. 33. 77.17. Friedberger, E. and Vallen, J. (1923): Klin. Wschr., 2, 1649.18. Wisseman, C. L. (1954): J. Clin. Invest., 33, 264.19. Cecil, R. L. and Loeb, R. F. (1959): A Textbook of Medicine, p. 614.Philadelphia: Saunders.20. Huckstep, R. L. (1962): Typhoid Fever and other Salmonella Infec-tions, p. 180. Edinburgh: Livingstone.THE ORGANIZATION OF RESUSCITATION AND CASUALTY SERVICES[part 2]ASPECTS OF FIRST AID WITH SPECIAL REFERENCE TO SUPPORT OF VITAL FUNCTIONSIN ROAD TRAFFIC INJURIESDR. MARTIN H{SoN HOLMDAHL, Associate Professor of Physiology; Chief, Department of Anaesthesiology,University Hospital, Uppsala, SwedenA general knowledge of first aid measures and their speedyapplication are among the most important factors for reducingthe alarmingly high accident mortality rate in modern in-dustrial society. .It has been estimated that there would be a reduction of20% in the accident mortality rate if traffic casualties weregiven proper treatment before arrival in hospi:al. As far backas 1957, over 100,000 people were killed during the yearthrough road accidents all over the world. Thus at least20,000 lives yt:arly could be saved simply by better first aidand care during treatment.1. Frequency of Severe Injuries in Road Traffic AccidentsIn all the categories of road users, head injuries are veryfrequent in accidents. In the series reviewed, the incidencevaries betwen 50% and 80%, while for thoracic injuries it wasbetween 10% and 40%. In the survey of traffic accidents inScandinavia, every second casualty had head injuries, and in69% of fatal accidents, this was the main cause of death.Thoracic injuries represent the second highest percentage offatal injuries, being the main cause of death in 13%. Injuriesto the upper and lower extremities were found in 30% and38% respectively but they contributed only 2·3% of the deaths.Of the fatal injuries, 31% died at the scene of the accidentand 10% during transport to hospital. In these two groups,out of 36 deaths with head injuries, in 16 there was obstructionof air passages with blood, mucus or gastric contents, and in10 this obstruction was the main cause of death, the cranio-cerebral and other injuries per se being considered compatiblewith life.Conclusion. In head and thoracic injuries, interference withthe respiration is an important factor contributing to a fataloutcome, and in many cases early elimination of this factormay save the victims. The rescuer must, therefore, have aclear knowledge of the mechanism of the interference withthe vital functions in order to give the casualty the bestpossible ch2n-~e of survival.2. Necessity for Immediate Support of RespirationWhenever there is a disturbance of consciousness, ventilationof the lungs may cease for no other reason than that the airpassage is no longer actively held open. The tongue is nolonger actively held in such a position that the air can passfreely and protective reflexes such as swallowing and closureof the larynx may not be functioning to prevent foreignmatter, e.g. blood, from blocking the pharynx or being in-haled. A cerebral trauma can directly influence and reducecentral respiratory activity, and damage to the thoracic cage,pleura or lungs will impair the normal mechanics of lungventilation. In acute obstruction of the airway (obstructiveasphyxia) the resistance of the brain to anoxia is all-important.Conclusion. The time available for relieving airway obstruc-tion and beginning artificial respiration in an accident withrespiratory difficulties is very short, since, owing to anoxia.other vital functions sometimes fail before the completecessation of respiratory movement. Speed is therefore of the

Acute haemolytic anaemia as a complication of thyphoid fever

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Acute haemolytic anaemia as a complication of thyphoid fever

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