Leptospirosis: A forgotten cause of quadriplegia

Abstract

Quadriplegia may be of acute, subacute, or chronic onset and may have varied etiologies. Leptospirosis can produce quadriplegia, secondary to hypokalemia, which occurs due to kaliuresis. Leptospirosis is under diagnosed and under reported in India. The clinical features of leptospirosis are non-specific. Combining clinical expertise and awareness with rapid tests for diagnosis will increase the recognition of patients with leptospirosis and hypokalemia. Renal involvement is common in leptospirosis. In our country, hypokalemic manifestations of leptospirosis are under reported. We report a case of quadriplegia due to hypokalemia, secondary to leptospirosis.

Keywords: Hypokalemia, leptospirosis, quadriplegia

How to cite this article:
Nattusamy L, Singh S. Leptospirosis: A forgotten cause of quadriplegia. Ann Trop Med Public Health 2012;5:603-4
How to cite this URL:
Nattusamy L, Singh S. Leptospirosis: A forgotten cause of quadriplegia. Ann Trop Med Public Health [serial online] 2012 [cited 2017 Nov 14];5:603-4. Available from: https://www.atmph.org/text.asp?2012/5/6/603/109306
Introduction

Leptospirosis is caused by pathogenic leptospires and is characterized by a broad spectrum of clinical manifestations, varying from inapparent infection to fulminant, fatal disease. Severe leptospirosis is characterized by jaundice, renal dysfunction, and hemorrhagic diathesis referred to as Weil’s syndrome. It is one of the most widespread zoonotic infection in world today, and it has long been considered a rare zoonotic disease in India with only sporadic cases being reported. [1] Renal involvement is common in leptospirosis. It is characterized by acute renal failure and the presence of hypokalemia with an elevated urinary fractional excretion of potassium. [2] We report a case of hypokalemic quadriplegia due to leptospirosis as it is rarely reported and early detection and management hastens the recovery.

Case Report

A 33-year-old male, outdoor manual worker, admitted with history of sudden onset of weakness of all 4 limbs of grade (1/5) of one-day duration. He had intermittent fever for 7 days. No previous history of muscle weakness. Blood pressure was normal. His higher functions, sensorium, cranial nerves, sensory system were normal. Deep tendon reflexes were diminished. Plantar-flexor response. Other systems examination was unremarkable. Chest x-ray and urine analysis was normal. Malarial parasite-negative. Blood sugar-was 104 mg, and serum sodium-138 Meq/L. Serum phosphate, magnesium, arterial blood gas analysis, liver function tests, ultrasound abdomen, and thyroid function tests were normal. Blood urea-44 mg, serum creatinine-1.2 mg, serum total and ionized calcium were normal. His hemogram was normal, except for total WBC count of 12,000 cells/cumm. Serum potassium was 2.4 Meq/L. Electrocardiogram (ECG) showed features of hypokalemia. Blood and urine culture were sterile. He tested positive for leptospirosis utilizing Macroscopic Slide Agglutination Test (MSAT) with titer of 3 +. His Modified Faine’s score was 30 (Clinical (A) + Environmental (B) + Laboratory (C)). [3],[4],[5] MSAT was confirmed by MAT (Microscopic Agglutination Test) with titers of ≥ 1:80. His urine potassium was 27 Meq/L, suggesting the renal loss of potassium. Transtubular potassium gradient was also suggestive of renal loss of potassium. No history of vomiting/loose stools/drug intake known to produce hypokalemia. Other common causes of fever were excluded. Patient was treated with intravenous crystalline penicillin 20 lakhs units every 6 th hourly along with parenteral potassium supplementation initially and subsequently with oral potassium supplementation. His motor power improved, and he was able to walk once the serum potassium normalized. ECG changes of hypokalemia normalized, and he was discharged on the 7 th day of hospitalization. He didn’t require further potassium supplementation on follow up visits and completely recovered from the illness.

Discussion

The kidneys are invariably involved in leptospirosis and findings range from urinary sediment changes (leukocytes, erythrocytes, and hyaline or granular casts in urine), mild proteinuria in anicteric leptospirosis to renal failure in severe disease. Renal failure occurs in the 2 nd week, but it can occur as early as on the 4 th day. Renal failure can be due to pre-renal component, acute interstitial nephritis, and acute tubular necrosis. Leptospires are nephrophilic and penetrates glomeruli, peritubular capillaries, interstitium, tubular lumen, ultimately leading to acute tubular necrosis and acute interstitial nephritis. The pathogenesis is related to the direct toxic effects of leptospiral compounds on renal transporters and microcirculation or to indirect effects of the pro-inflammatory response with severe damage. [2],[6] Tubular dysfunction is a hallmark of severe leptospirosis and anti-microbial therapy interferes on the renal involvement. Bacterial invasion, inflammatory process, hemodynamic alterations, and direct toxicity of bacterial products are thought to be responsible for the development of nephropathy. Bacterial products, especially the outer membrane proteins consisting of OmpL1, LipL41, and LipL36 are toxic to the kidneys. [6],[7] OmpL1, lipoprotein LipL41, and lipopolysaccharide are exposed on the surface of leptospires. Pathogenic leptospires colonizes the proximal tubular epithelial cells and glycolipoprotein by its incorporation with the cell membrane causes renal tubular and vascular endothelial damage. Pathologically all renal structures are involved. [8] It is a potent inhibitor of Na-K + ATPase of renal tubular epithelial cells. [6] The resulting increase of intra-cellular Na + decreases Na + transport at the luminal border of all parts of renal tubules. Increased Na + delivery to the collecting ducts for Na-K + exchange causes kaliuresis. Increased plasma aldosterone and cortisol levels further enhance K + excretion. There is also evidence of inhibition of Na-K + -2Cl co-transport in the medullary thick ascending limb of Henle’s loop. [6]

Hypokalemia caused by kaliuresis is noted in 26%- 40% of patients with leptospirosis and if it is significant, can lead to muscular weakness and in severe cases, lead to quadriplegia. [2],[9] Respiratory muscle weakness due to severe hypokalemia can be fatal. Our patient presented with the fever and quadriplegia. Evaluation of fever showed leptospirosis is the cause of fever, and hypokalemia is due to renal loss of potassium as evidenced by significant kaliuresis in our case. Hypokalemia produced the quadriplegia, which improved with appropriate management. This case is being presented to highlight the infectious diseases, especially leptospirosis as one of the important cause of fever with quadriplegia and hypokalemia as it is uncommonly reported.

Conclusion

We recommend that all patients with fever presenting with hypokalemia be investigated for leptospirosis, especially in endemic areas. Early identification of leptospirosis with hypokalemia can decrease the mortality.

References
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2. Abdulkader RC, Seguro AC, Malheiro PS, Burdmann EA, Marcondes M. Peculiar electrolytic and hormonal abnormalities in acute renal failure due to leptospirosis. Am J Trop Med Hyg 1996;54:16.
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6. Younes-Ibrahim M, Burth P, Faris MV, Buffin-Meyer B, Marsy S, Barlet-Bas C, et al. Inhibition of Na K-ATPase by endotoxin extracted from Leptospira interrogans: A possible mechanism for the pathophysiology of leptospirosis. C R Acad Sci III 1995;31:619-25.
7. Yang CW, Wu MS, Pan MJ, Hong JJ, Yu CC, Vandewalle A, et al. Leptospire outer membrane protein activates NF-kB and downstream genes expressed in medullary thick ascending limb cells. J Am Soc Nephrol 2000;11:2017-26.
8. Sitprija V, Evans H. The kidney in human leptospirosis. Am J Med 1970;49:780-8.
9. Seguro AC, Lomar AV, Rocha AS. Acute renal failure of leptospirosis: Nonoliguric and hypokalemic forms. Nephron 1990;55:146-51.

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/1755-6783.109306

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