Case Report
“Dry” and “wet” beriberi mimicking critical illness polyneuropathy S. Rama Prakasha, A. Sharik Mustafa1, Shashidhar Baikunje2, K. Subramanyam3 Departments of General Medicine, 1Neurology, 2Department of Nephrology, 3Department of Cardiology, K. S. Hegde Medical Academy, Deralakatte, Mangalore, Karnataka, India Abstract Three cases with manifestations of right heart failure, shock, metabolic acidosis, and renal failure in varying combination were admitted with paraparesis. Nerve conduction study suggested predominantly motor and mainly axonal type of neuropathy. Rapid reversal of shock, acidosis, and multi‑organ dysfunction with timely infusion of thiamine was followed by the complete neurological recovery.
Key Words Beri‑beri, critical illness polyneuropathy, multiorgan failure, thiamine For correspondence: Dr. S. Rama Prakasha, Department of General Medicine, K. S. Hegde Medical Academy, Deralakatte, Mangalore ‑ 575 018,
Karnataka, India. E‑mail: [email protected]
Ann Indian Acad Neurol 2013;16:687‑89
Introduction
Case Reports
Beriberi is the clinical disease associated with thiamine deficiency and sub‑acute thiamine deficiency will have symptoms of peripheral edema and mixed motor and sensory neuropathy. A more rapid form of wet beriberi is termed as acute fulminant cardiovascular beriberi or Shoshin beriberi, which manifests in the form of shock, severe metabolic acidosis, and renal failure. In individuals without risk‑factors for thiamine deficiency, the diagnosis of this condition is often missed.
Case 1 A 44‑year‑old non‑alcoholic male was admitted with dyspnea, vomiting, upper abdominal pain, oliguria, and weakness of both the lower limbs of 3 days duration. He was admitted thrice in the previous 1 month for symptoms of heart failure at a peripheral hospital, with partial recovery each time upon conservative treatment. On admission, patient had tachypnea, unrecordable blood pressure, heart rate 136/min, elevated Jugular Venous Pressure (JVP), and bilateral pitting edema of legs. Systemic examination revealed right sided S3, systolic murmur of 3/6 intensity at the lower left sternal edge and 3 cm tender hepatomegaly. Bilateral lower limb power was 3/5 with sluggish deep tendon reflexes.
C ri t i c a l i l l n e ss p o l y n e u r o p a t h y ( C I P ) i s a n a cu t e neuromuscular disorder of severely ill patients in the setting of systemic inflammatory response syndrome, sepsis, and multiple organ failure. In a patient with tachycardia, tachypnoea, and multiorgan dysfunction, weakness may be attributed to CIP, severe electrolyte disturbance, critical illness myopathy, pre‑existing neuropathy or possibly Guillain‑Barré syndrome (GBS). In this case series, we describe three patients who had the above manifestations and all had an uneventful recovery on treatment with intravenous thiamine. Access this article online Quick Response Code:
Website: www.annalsofian.org
DOI: 10.4103/0972-2327.120467
Electrocardiography (ECG) revealed sinus tachycardia with ST depression in leads V3‑V6. Arterial Blood Gas analysis showed severe metabolic acidosis [Table 1]. 2D echocardiography on admission showed dilated Right atrium/ Right ventricle (RA/RV) with mild tricuspid regurgitation and pulmonary hypertension [Table 1]. A provisional diagnosis of right heart failure with the multiorgan dysfunction possibly due to sepsis or cardiac beriberi was made and he was managed conservatively with broad spectrum antibiotics, sodium bicarbonate infusion, inotropes, and thiamine infusion. Acidosis, shock, and renal failure recovered promptly over from 24 h to 48 h. However, his paraparesis worsened over the next 2‑3 days and Nerve conduction study (NCS) suggested predominantly motor, axonal type of peripheral neuropathy [Table 2]. With continued thiamine supplementation, his power in the lower limbs gradually
Annals of Indian Academy of Neurology, October-December 2013, Vol 16, Issue 4
Prakasha, et al.: Beriberi mimicking critical illness polyneuropathy
688
Table 1: Investigation reports Parameter Hemoglobin TLC (on admission)/mm3 Platelet count/mm3 Creatinine (max) Urea (max) SGOT/SGPT Albumin (on admission) CPK/CPK-MB Sodium Potassium pH: On admission pH: On second day HCO3: On admission HCO3: On second day 2D echocardiography
Case 1
Case 2
Case 3
Normal value
13.6 7600 253,000 4.35 130 91/51 4.1 494/51 131 7.6 6.94 7.421 3.3 24.8 RA/RV dilatation, Mild TR, PASP‑50 mm of Hg
11.3 10,600 453,000 1.34 61 64/36 3.6 1208/29 132 4.9 7.28 7.42 14.3 23.2 Mild TR, PASP‑40 mm of Hg, Normal cardiac chamber dimensions
14.2 8,400 35,000 1.9 151 47/64 4.3 303/11 124.6 5.4 7.26 7.42 13.2 22.6 Dilated RA/RV, Moderate TR, PASP 50 mm of Hg
13‑16 g/dl 4000‑11,000 150,000‑400,000
“Dry” and “wet” beriberi mimicking critical illness polyneuropathy S. Rama Prakasha, A. Sharik Mustafa1, Shashidhar Baikunje2, K. Subramanyam3 Departments of General Medicine, 1Neurology, 2Department of Nephrology, 3Department of Cardiology, K. S. Hegde Medical Academy, Deralakatte, Mangalore, Karnataka, India Abstract Three cases with manifestations of right heart failure, shock, metabolic acidosis, and renal failure in varying combination were admitted with paraparesis. Nerve conduction study suggested predominantly motor and mainly axonal type of neuropathy. Rapid reversal of shock, acidosis, and multi‑organ dysfunction with timely infusion of thiamine was followed by the complete neurological recovery.
Key Words Beri‑beri, critical illness polyneuropathy, multiorgan failure, thiamine For correspondence: Dr. S. Rama Prakasha, Department of General Medicine, K. S. Hegde Medical Academy, Deralakatte, Mangalore ‑ 575 018,
Karnataka, India. E‑mail: [email protected]
Ann Indian Acad Neurol 2013;16:687‑89
Introduction
Case Reports
Beriberi is the clinical disease associated with thiamine deficiency and sub‑acute thiamine deficiency will have symptoms of peripheral edema and mixed motor and sensory neuropathy. A more rapid form of wet beriberi is termed as acute fulminant cardiovascular beriberi or Shoshin beriberi, which manifests in the form of shock, severe metabolic acidosis, and renal failure. In individuals without risk‑factors for thiamine deficiency, the diagnosis of this condition is often missed.
Case 1 A 44‑year‑old non‑alcoholic male was admitted with dyspnea, vomiting, upper abdominal pain, oliguria, and weakness of both the lower limbs of 3 days duration. He was admitted thrice in the previous 1 month for symptoms of heart failure at a peripheral hospital, with partial recovery each time upon conservative treatment. On admission, patient had tachypnea, unrecordable blood pressure, heart rate 136/min, elevated Jugular Venous Pressure (JVP), and bilateral pitting edema of legs. Systemic examination revealed right sided S3, systolic murmur of 3/6 intensity at the lower left sternal edge and 3 cm tender hepatomegaly. Bilateral lower limb power was 3/5 with sluggish deep tendon reflexes.
C ri t i c a l i l l n e ss p o l y n e u r o p a t h y ( C I P ) i s a n a cu t e neuromuscular disorder of severely ill patients in the setting of systemic inflammatory response syndrome, sepsis, and multiple organ failure. In a patient with tachycardia, tachypnoea, and multiorgan dysfunction, weakness may be attributed to CIP, severe electrolyte disturbance, critical illness myopathy, pre‑existing neuropathy or possibly Guillain‑Barré syndrome (GBS). In this case series, we describe three patients who had the above manifestations and all had an uneventful recovery on treatment with intravenous thiamine. Access this article online Quick Response Code:
Website: www.annalsofian.org
DOI: 10.4103/0972-2327.120467
Electrocardiography (ECG) revealed sinus tachycardia with ST depression in leads V3‑V6. Arterial Blood Gas analysis showed severe metabolic acidosis [Table 1]. 2D echocardiography on admission showed dilated Right atrium/ Right ventricle (RA/RV) with mild tricuspid regurgitation and pulmonary hypertension [Table 1]. A provisional diagnosis of right heart failure with the multiorgan dysfunction possibly due to sepsis or cardiac beriberi was made and he was managed conservatively with broad spectrum antibiotics, sodium bicarbonate infusion, inotropes, and thiamine infusion. Acidosis, shock, and renal failure recovered promptly over from 24 h to 48 h. However, his paraparesis worsened over the next 2‑3 days and Nerve conduction study (NCS) suggested predominantly motor, axonal type of peripheral neuropathy [Table 2]. With continued thiamine supplementation, his power in the lower limbs gradually
Annals of Indian Academy of Neurology, October-December 2013, Vol 16, Issue 4
Prakasha, et al.: Beriberi mimicking critical illness polyneuropathy
688
Table 1: Investigation reports Parameter Hemoglobin TLC (on admission)/mm3 Platelet count/mm3 Creatinine (max) Urea (max) SGOT/SGPT Albumin (on admission) CPK/CPK-MB Sodium Potassium pH: On admission pH: On second day HCO3: On admission HCO3: On second day 2D echocardiography
Case 1
Case 2
Case 3
Normal value
13.6 7600 253,000 4.35 130 91/51 4.1 494/51 131 7.6 6.94 7.421 3.3 24.8 RA/RV dilatation, Mild TR, PASP‑50 mm of Hg
11.3 10,600 453,000 1.34 61 64/36 3.6 1208/29 132 4.9 7.28 7.42 14.3 23.2 Mild TR, PASP‑40 mm of Hg, Normal cardiac chamber dimensions
14.2 8,400 35,000 1.9 151 47/64 4.3 303/11 124.6 5.4 7.26 7.42 13.2 22.6 Dilated RA/RV, Moderate TR, PASP 50 mm of Hg
13‑16 g/dl 4000‑11,000 150,000‑400,000
