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Congestive heart failure in the course of typhoid fever
Journal of Infection (I982) 4, 81-84
CASE REPORT Congestive
heart failure in the course of typhoid
fever
M . S h a l i t , * A. J. B r a v e r m a n a n d M . E l i a k i m
Department of Medicine A, Hadassah University Hospital, Jerusalem, Israel Summary A young patient who developed congestive heart failure in the course of typhoid fever is described. Numberous electrocardiograms revealed no or minimal changes. The possible cause of this rare complication is discussed. Introduction Electrocardiographic abnormalities in t y p h o i d fever are frequent 1-6 and usually consist of flattening or inversion of the T waves, depression of the S T segment, disturbances in r h y t h m and S T elevation consistent with pericarditis. Inflammatory, toxic and metabolic factors have been implicated in the aetiology of these changes. 2, ~, 7 T h e electrocardiographic abnormalities are usually not associated with clinical signs of myocarditis, although softening of the heart sounds, tachycardia and h y p o t e n s i o n have been reportedY. 8 Congestive heart failure is extremely rare and, to the best of our knowledge, only six cases have so far been reported. 9-11 T h e present paper describes a patient with t y p h o i d fever w h o developed severe congestive heart failure with minimal electrocardiographic changes; additional complication were present as well.
Case report A I 6 - y e a r - o l d male of K u r d i s h origin was admitted to the D e p a r t m e n t of Medicine A with fever, chills and jaundice of IO days duration. Physical examination revealed an acutely ill confused patient with jaundice. T h e t e m p e r a t u r e was 40 °C, the pulse I2O per minute and the b l o o d pressure 120/18o m m H g . T h e r e were no abnormal findings in the lungs and heart. T h e liver was palpable 4 cm and the spleen I cm below the costal margin. Rose spots were seen on the chest and abdomen. Neurological examination was normal.
Laboratory tests T h e erythrocyte sedimentation rate was 30/65 m m after one and two hours (Westergren), the leucocyte count was 9"6 x IO9/1 with a shift to the left, haemoglobin was lO. 4 g / d l , platelet count 15o x io9/1. Blood urea nitrogen, s e r u m creatinine and uric acid were normal. S e r u m bilirubin was I36 #mol/1, of which 5I # m o l / l was conjugated. S G O T was 53I m U / m l , alkaline phosphatase 3oo m U / m l , L D H 335o m U / m l , albumin 27 g/1 and globulin 32 g/1. Plasma haemoglobin was 27o m g / d l . T h e Widal test was positive at a titre of I :4oo and b l o o d cultures grew Salmonella typhi. T h e red cells were f o u n d to * Correspondence to M. Shalit. oi63-4483/82/oioo8I +06 $oi.oo/o
© I982 The British Society for the Study of Infection
82
M. SHALIT,
A. J. B R A V E R M A N N
AND
I
It
III
R
k
F
M. ELIAKIM
VI
V6
V4
Fig. I (a). Electrocardiogram on admission.
I
II
Ill
R
k
F
VI
V2
V4
V5
V6
Fig. I (b). Electrocardiogram on the 5th day. Note slight S T elevation and tall peaked T waves in leads V2-V ~. Serum potassium was 4 m E q / 1 .
be deficient in glucose 6-phosphate dehydrogenase. Urinalysis showed excretion of 2"3 g protein per 24 hours, haemoglobin 44, 5-1o leucocytes and many granular casts per high power field. T h e electrocardiogram (Fig. I a) and chest X-ray film on admission (Plate I a) were normal. A liver biopsy showed typical ' typhoid nodules '.
~ournal of Infection
Plate r
Plate I (a). Chest X-ray film on admission.
Plate r (b). Chest X-ray film on the 5th day. Note cardiomegaly and right pleural effusion.
M. SHALIT ET AL.
(Facing p. 82)
Journal of Infection
Plate I
Plate I (c). Chest X-ray film after recovery. Note n o r m a l heart size a n d disappearance of pleural effusion.
M. SHALIT E T
AL.
Heart failure in typhoid fever
83
T r e a t m e n t consisted of chloramphenical 3"o g per day. O n the third hospital day, the haemoglobin was 8"3 g / d l , the reticulocyte count I per cent and the patient was given two units of packed cells. O n the 5th day, the patient d e v e l o p e d severe dyspnoea. Physical examination disclosed e n g o r g e m e n t o f the neck veins (venous pressure 24 cm), weakening of the heart sounds with dullness on percussion over the right base and crepitant tales over b o t h bases. A chest X - r a y film revealed marked cardiomegaly, p u l m o n a r y congestion and right pleural effusion (Plate r b). T h e electrocardiogram showed a slight elevation of the S T segment and tall T waves (Fig. I b). Echocardiography s h o w e d no evidence of pericardial effusion. Right pleural p u n c t u r e revealed straw-coloured fluid with a protein content of I7 g/l. T h e findings described above were diagnostic of congestive heart failure and the patient was started on digoxin and frusemide. D u r i n g the next few days, his condition i m p r o v e d ; an additional chest film revealed regression of the cardiomegaly and the p u l m o n a r y congestion (Plate r c). Later on, the clinical and laboratory findings o f liver and kidney involvement and the haemolysis disappeared and the patient was discharged in a satisfactory condition after 18 days. Discussion
T h i s patient manifested several of the complications e n c o u n t e r e d in t y p h o i d fever, namely acute haemolysis with haemoglobinuria, hepatitis, nephritis and, most of all, severe congestive heart failure. T h e presence of heart failure in t y p h o i d fever has been ascribed either to myocarditis or endocarditis. 9-n It is of interest that three of the five patients in one report n were initially diagnosed as suffering from rheumatic fever, while the fourth was believed to have b r o n c h o p n e u m o n i a . Congestive heart failure was the presenting s y m p t o m in all of these cases. O u r patient developed heart failure at the beginning of the third week of the disease and made a complete recovery. Interestingly, n u m e r o u s electrocardiograms s h o w e d no alterations and minimal changes were observed in only one record (Plate r b), neither were there any clinical signs of pericarditis or endocarditis. T h e patient had overt haemolysis b u t his h a e m o g l o b i n level did not fall b e l o w 8.o g/dl. T h e renal and heptic involvement was not considered the cause of fluid retention sufficient to compromise heart function. It is m o t likely, therefore, that myocarditis was the cause of cardiac failure while other complications might be contributory factors. References
I. Porter WB, Bloom N. The heart in typhoid fever. Am Heart J 1935; xo: 793-797. 2. Stuart BM, Pullen RL. Typhoid: clinical analysis of three hundred and sixty cases. Arch lnt Med I946; 78: 629-66I. 3. Mainzer F. Electrocardiographic study of typhoid myocarditis. Br HeartJ I947; 9:145-153 4. Rachmilewitz M, Braun K. Electrocardiographic changes in typhoid fever and their reversibility following niacin treatment. Am Heart J I948; 36: 284-294. 5. Eliakim M. Electrocardiographic signs of pericarditis in typhoid fever. A m J filed Sci 196o; 239: 492-497. 6. Gulati PD, Saxena SN, Bact D, Gupta PS, Chuttani HK. Changing pattern of typhoid fever. Am J Med 1968; 45: 544-548. 7. Rowland HAK. The complications of typhoid fever. J Trop Med Hyg 1961; 64: 143-152.
84
M. SHALIT~ A. J. B R A V E R M A N N AND M. E L I A K I M
8. Bertrand E, Barabe P, Odi-Assamoi M. La Myocardite typhoidique. Coeur Med Interne I 9 7 I ; IO" 2 1 3 - 2 2 0 .
9. Le Van Diem, Arnold K. Typhoid fever with myocarditis, dim J Trop Med Hyg I974; 23: 218--22I.
Io. Mokhobo KP. Typhoid cardiac involvement. S difr M e d J I975; 49: 55-56. xL Mokhobo KP. Typhoid cardiac involvement. S difr M e d J I975; 49: 728.
CASE REPORT Congestive
heart failure in the course of typhoid
fever
M . S h a l i t , * A. J. B r a v e r m a n a n d M . E l i a k i m
Department of Medicine A, Hadassah University Hospital, Jerusalem, Israel Summary A young patient who developed congestive heart failure in the course of typhoid fever is described. Numberous electrocardiograms revealed no or minimal changes. The possible cause of this rare complication is discussed. Introduction Electrocardiographic abnormalities in t y p h o i d fever are frequent 1-6 and usually consist of flattening or inversion of the T waves, depression of the S T segment, disturbances in r h y t h m and S T elevation consistent with pericarditis. Inflammatory, toxic and metabolic factors have been implicated in the aetiology of these changes. 2, ~, 7 T h e electrocardiographic abnormalities are usually not associated with clinical signs of myocarditis, although softening of the heart sounds, tachycardia and h y p o t e n s i o n have been reportedY. 8 Congestive heart failure is extremely rare and, to the best of our knowledge, only six cases have so far been reported. 9-11 T h e present paper describes a patient with t y p h o i d fever w h o developed severe congestive heart failure with minimal electrocardiographic changes; additional complication were present as well.
Case report A I 6 - y e a r - o l d male of K u r d i s h origin was admitted to the D e p a r t m e n t of Medicine A with fever, chills and jaundice of IO days duration. Physical examination revealed an acutely ill confused patient with jaundice. T h e t e m p e r a t u r e was 40 °C, the pulse I2O per minute and the b l o o d pressure 120/18o m m H g . T h e r e were no abnormal findings in the lungs and heart. T h e liver was palpable 4 cm and the spleen I cm below the costal margin. Rose spots were seen on the chest and abdomen. Neurological examination was normal.
Laboratory tests T h e erythrocyte sedimentation rate was 30/65 m m after one and two hours (Westergren), the leucocyte count was 9"6 x IO9/1 with a shift to the left, haemoglobin was lO. 4 g / d l , platelet count 15o x io9/1. Blood urea nitrogen, s e r u m creatinine and uric acid were normal. S e r u m bilirubin was I36 #mol/1, of which 5I # m o l / l was conjugated. S G O T was 53I m U / m l , alkaline phosphatase 3oo m U / m l , L D H 335o m U / m l , albumin 27 g/1 and globulin 32 g/1. Plasma haemoglobin was 27o m g / d l . T h e Widal test was positive at a titre of I :4oo and b l o o d cultures grew Salmonella typhi. T h e red cells were f o u n d to * Correspondence to M. Shalit. oi63-4483/82/oioo8I +06 $oi.oo/o
© I982 The British Society for the Study of Infection
82
M. SHALIT,
A. J. B R A V E R M A N N
AND
I
It
III
R
k
F
M. ELIAKIM
VI
V6
V4
Fig. I (a). Electrocardiogram on admission.
I
II
Ill
R
k
F
VI
V2
V4
V5
V6
Fig. I (b). Electrocardiogram on the 5th day. Note slight S T elevation and tall peaked T waves in leads V2-V ~. Serum potassium was 4 m E q / 1 .
be deficient in glucose 6-phosphate dehydrogenase. Urinalysis showed excretion of 2"3 g protein per 24 hours, haemoglobin 44, 5-1o leucocytes and many granular casts per high power field. T h e electrocardiogram (Fig. I a) and chest X-ray film on admission (Plate I a) were normal. A liver biopsy showed typical ' typhoid nodules '.
~ournal of Infection
Plate r
Plate I (a). Chest X-ray film on admission.
Plate r (b). Chest X-ray film on the 5th day. Note cardiomegaly and right pleural effusion.
M. SHALIT ET AL.
(Facing p. 82)
Journal of Infection
Plate I
Plate I (c). Chest X-ray film after recovery. Note n o r m a l heart size a n d disappearance of pleural effusion.
M. SHALIT E T
AL.
Heart failure in typhoid fever
83
T r e a t m e n t consisted of chloramphenical 3"o g per day. O n the third hospital day, the haemoglobin was 8"3 g / d l , the reticulocyte count I per cent and the patient was given two units of packed cells. O n the 5th day, the patient d e v e l o p e d severe dyspnoea. Physical examination disclosed e n g o r g e m e n t o f the neck veins (venous pressure 24 cm), weakening of the heart sounds with dullness on percussion over the right base and crepitant tales over b o t h bases. A chest X - r a y film revealed marked cardiomegaly, p u l m o n a r y congestion and right pleural effusion (Plate r b). T h e electrocardiogram showed a slight elevation of the S T segment and tall T waves (Fig. I b). Echocardiography s h o w e d no evidence of pericardial effusion. Right pleural p u n c t u r e revealed straw-coloured fluid with a protein content of I7 g/l. T h e findings described above were diagnostic of congestive heart failure and the patient was started on digoxin and frusemide. D u r i n g the next few days, his condition i m p r o v e d ; an additional chest film revealed regression of the cardiomegaly and the p u l m o n a r y congestion (Plate r c). Later on, the clinical and laboratory findings o f liver and kidney involvement and the haemolysis disappeared and the patient was discharged in a satisfactory condition after 18 days. Discussion
T h i s patient manifested several of the complications e n c o u n t e r e d in t y p h o i d fever, namely acute haemolysis with haemoglobinuria, hepatitis, nephritis and, most of all, severe congestive heart failure. T h e presence of heart failure in t y p h o i d fever has been ascribed either to myocarditis or endocarditis. 9-n It is of interest that three of the five patients in one report n were initially diagnosed as suffering from rheumatic fever, while the fourth was believed to have b r o n c h o p n e u m o n i a . Congestive heart failure was the presenting s y m p t o m in all of these cases. O u r patient developed heart failure at the beginning of the third week of the disease and made a complete recovery. Interestingly, n u m e r o u s electrocardiograms s h o w e d no alterations and minimal changes were observed in only one record (Plate r b), neither were there any clinical signs of pericarditis or endocarditis. T h e patient had overt haemolysis b u t his h a e m o g l o b i n level did not fall b e l o w 8.o g/dl. T h e renal and heptic involvement was not considered the cause of fluid retention sufficient to compromise heart function. It is m o t likely, therefore, that myocarditis was the cause of cardiac failure while other complications might be contributory factors. References
I. Porter WB, Bloom N. The heart in typhoid fever. Am Heart J 1935; xo: 793-797. 2. Stuart BM, Pullen RL. Typhoid: clinical analysis of three hundred and sixty cases. Arch lnt Med I946; 78: 629-66I. 3. Mainzer F. Electrocardiographic study of typhoid myocarditis. Br HeartJ I947; 9:145-153 4. Rachmilewitz M, Braun K. Electrocardiographic changes in typhoid fever and their reversibility following niacin treatment. Am Heart J I948; 36: 284-294. 5. Eliakim M. Electrocardiographic signs of pericarditis in typhoid fever. A m J filed Sci 196o; 239: 492-497. 6. Gulati PD, Saxena SN, Bact D, Gupta PS, Chuttani HK. Changing pattern of typhoid fever. Am J Med 1968; 45: 544-548. 7. Rowland HAK. The complications of typhoid fever. J Trop Med Hyg 1961; 64: 143-152.
84
M. SHALIT~ A. J. B R A V E R M A N N AND M. E L I A K I M
8. Bertrand E, Barabe P, Odi-Assamoi M. La Myocardite typhoidique. Coeur Med Interne I 9 7 I ; IO" 2 1 3 - 2 2 0 .
9. Le Van Diem, Arnold K. Typhoid fever with myocarditis, dim J Trop Med Hyg I974; 23: 218--22I.
Io. Mokhobo KP. Typhoid cardiac involvement. S difr M e d J I975; 49: 55-56. xL Mokhobo KP. Typhoid cardiac involvement. S difr M e d J I975; 49: 728.