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Year : 2014  |  Volume : 19  |  Issue : 2  |  Page : 144-147

Acute hypopituitarism - a rare complication of vasculotoxic snake bite: A case report

Department of Medicine, Mahatma Gandhi Institute of Medical Sciences, Sevagram, Wardha, Maharashtra, India

Date of Web Publication11-Aug-2014

Correspondence Address:
Amrish Saxena
Department of Medicine, Mahatma Gandhi Institute of Medical Sciences, Sevagram, Wardha - 442 102, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9903.138440

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Venomous snake bite is an important public health hazard in tropical countries including India. Vasculotoxic snake bites are well known to cause local cellulitis, local tissue necrosis, bleeding manifestations, disseminated intravascular coagulation (DIC), acute kidney injury (AKI), shock, cardiac arrhythmia, neurotoxicity, coma, and death. We present the case of a 30-year-old female who was bitten by a Russell's viper snake and complicated by AKI, DIC, and acute hypopituitarism during her hospital course. Acute hypopituitarism as a complication of snake bite is a rare entity.

Keywords: Acute kidney injury, disseminated intravascular coagulation, hypopituitarism, snake bite

How to cite this article:
Saxena A, Srivastava AK, Rajput AS, Tiewsoh I, Jajoo UN. Acute hypopituitarism - a rare complication of vasculotoxic snake bite: A case report. J Mahatma Gandhi Inst Med Sci 2014;19:144-7

How to cite this URL:
Saxena A, Srivastava AK, Rajput AS, Tiewsoh I, Jajoo UN. Acute hypopituitarism - a rare complication of vasculotoxic snake bite: A case report. J Mahatma Gandhi Inst Med Sci [serial online] 2014 [cited 2023 Mar 30];19:144-7. Available from: https://www.jmgims.co.in/text.asp?2014/19/2/144/138440

  Introduction Top

In India more than 200,000 snake bites are reported annually, of which 35,000-50,000 lives are lost due to venomous snake bites. [1] Snake bites by Russell's viper can cause vasculotoxicity, neurotoxicity, or myotoxicity. The usual complications of viper bites mentioned in the literature are local cellulitis, hemorrhagic manifestations, disseminated intravascular coagulation (DIC), acute renal failure (ARF), intravascular hemolysis, pulmonary edema, shock, cardiac arrhythmia, neurotoxicity (ptosis, external ophthalmoplegia, muscle paralysis, and cerebrovascular stroke), and death. [1],[2] Bleeding manifestations and acute kidney injury (AKI) are common events following bites by Russell's viper but acute hypopituitarism as a complication of vasculotoxic snake bite is a rare sequelae.

Here, we report a case of young female who was bitten by Russell's viper and complicated by ARF and DIC. She developed recurrent hypoglycemia and hypotension during her hospital course as a consequence of acute hypopituitarism secondary to snake bite.

  Case Report Top

A 30-year-old woman, a field worker was bitten by a snake on her right hand ring finger. The villagers identified the snake as Russell's viper. She was admitted in hospital after 2 h of snake bite. On general examination, she was conscious, oriented with a pulse rate of 106 beats per min, blood pressure (BP) of 110/70 mmHg, and a respiratory rate of 18 breaths per min. A local swelling was present on the ring finger of right hand. Her 20 min whole blood clotting test (WBCT) was of good quality at the time of admission. No lymphadenopathy was present. Her fundus examination and systemic examination revealed no abnormality. No signs of neurotoxicity were present. After 3 h of admission, she had an episode of hematemesis associated with mild pain in abdomen, palpitations, and restlessness. Her BP dropped down to 80/60 mmHg with a pulse rate of 114 per min. Her repeat 20 min WBCT was of poor quality (incoagulable blood). She was given 10 vials (100 units) of polyvalent anti-snake venom (ASV) intravenously over 1 h, covering four common species; Russell's viper, common cobra, common krait, and saw-scaled viper. In view of her hypotension, intravenous noradrenalin infusion was started after adequate intravenous fluid replacement. She had bleeding manifestations in the form of gum bleeding, epistaxis, hematemesis, ecchymoses, and subconjunctival hemorrhages. Her 20 min WBCT repeated after 6 h of admission was also of poor quality. She was given another 10 vials (100 units) of polyvalent ASV.

Her hemogram on the day of admission showed a hemoglobin of 13.6 gm/dL, total leukocyte count of 9,200 mm 3 (with differential of 79% polymorphonuclear leukocytes, 13% lymphocytes), and platelet count of 270,000 mm 3 . Other laboratory test results were serum creatinine, 2.1 mg/dL; urea, 48 mg/dL; sodium, 140 mEq/L; potassium, 4.3 mEq/L; aspartate aminotransferase (AST), 233 IU/L; alanine aminotransferase (ALT), 671 IU/L; total bilirubin, 0.44 mg/dL; albumin, 3.16 gm/dL; and total protein, 6.7 gm/dL. The urinalysis demonstrated proteinuria (2+) on albustick. Abdominal ultrasonography (USG) revealed no obvious abnormality.

Her urine output was less than 100 mL over 24 h of admission. She developed puffiness on face and peripheral edema. In view of rising renal parameters; oliguria, pulmonary edema, and hypotension, she was put on peritoneal dialysis. Next day, her BP improved to 110/70 mmHg. Later, she underwent four sessions of intermittent hemodialysis. Gradually her renal parameters were improved and her urine output was improved to 800 mL/day [Table 1].
Table 1: Laboratory test results during patient's hospital course (patient was admitted on 29th September)

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Meanwhile, she had recurrent episodes of hypoglycemia during her hospital course [Table 1]. Her hypoglycemic episodes were associated with sweating, anxiety, tremors, mental confusion, and palpitations. She also had two episodes of generalized tonic-clonic seizures (GTCS) associated with documented hypoglycemia. These episodes responded well to intravenous dextrose. There was no history of intake of any oral hypoglycemic medications or insulin which can be attributable to her hypoglycemia. Her oxygen saturation measured by pulse oximetry was normal during seizures. Her serum electrolytes including sodium, calcium, and magnesium levels were also within normal limits at the time of seizures. Similarly, recurrent hypotension was also recorded during her hospital course. The possible causes which can be attributable to her hypoglycemia are insulinoma causing hyperinsulinemia or a disturbance of the hypothalamic-pituitary axis or its target organs (pituitary/adrenal insufficiency) or underlying sepsis. The patient was investigated accordingly. Her hormonal profile revealed (reference values in bracket) insulin 2.16 μIU/mL (fasting level: 2-25), cortisol at 8.00 AM (repeated twice) 2.53 and 2.17 μg/dL (6.2-19.4), thyroid stimulating hormone (TSH) 0.02 μIU/mL (0.30-5.5), free thyroxine (T4) 0.52 ng/dL (0.70-1.80), free triiodothyronine (T3) 0.8 pg/mL (1.7-4.2), growth hormone 0.16 ng/mL (up to 8 ng/mL), and prolactin 1.8 ng/mL (2.0-25.0). Results of serum hormone estimation confirmed the deficiency of hormones secreted from the pituitary and its target organs. Her coagulation profile revealed prolonged prothrombin time, partial thromboplastin time, and high levels of fibrin degradation products in plasma. Her repeated platelet count dropped to 14,000/mm 3 [Table 1]. Her blood cultures sent twice were negative. The magnetic resonance imaging (MRI) of brain without contrast revealed a normal pituitary gland and no evidence of intracranial bleed.

A final diagnosis of Russell's viper snake bite complicated by AKI, DIC, and acute hypopituitarism was made. A diagnosis of DIC was made in view of low platelet count, increased fibrin degradation products in serum, and clinical evidence of bleeding. She was started hydrocortisone 100 mg intravenously 6 hourly and later shifted to oral prednisolone 30 mg/day. L-thyroxine 50 μg daily was added. She received fresh frozen plasma to replace depleted clotting factors and platelet concentrates to correct thrombocytopenia. Intravenous antibiotics were added. She gradually recovered from AKI and her recurrent hypoglycemia and hypotension responded well to corticosteroids.

After 2 weeks of her discharge, she was again admitted with complaints of giddiness and one episode of seizure. Her blood sugar recorded was 54 mg/dL and BP was 90/60 mmHg. Her oral prednisolone dose was tapered from 30 to 20 mg 2 days prior to this episode of seizure. After this episode, the dose of prednisolone was again increased to 30 mg/day and continued for next 6 weeks. The serum creatinine and blood urea repeated 1 month after her discharge were 1.4 and 32 mg/dL, respectively. Her serum free T4 and free T3 were 0.84 ng/dL and 1.49 pg/mL, respectively after 1 month of starting thyroxine 50 μg per day. After getting the suboptimal response, her thyroxine dose was escalated to 100 μg per day. On 1 month follow-up visit after her initial discharge, her follicle stimulating hormone (FSH) and estradiol hormone were found to be low, that is, 0.6 mIU/mL (3-20 mIU/mL) and 12 pg/mL (20-145 pg/ mL), respectively. Her gonadal hormonal tests were not done during her initial hospitalization due to financial constraints. She was supplemented with oral estrogen 1 mg daily for 25 days and oral progesterone 5 mg daily on days 16-25 of menstrual cycle as hormonal replacement. During hospitalization or follow-up after discharge, patient did not develop any symptoms suggestive of posterior pituitary involvement. Hence, posterior pituitary hormonal tests (vasopressin levels) were not done. Her prednisolone dose was tapered to 5 mg on subsequent follow-up visits and there was improvement in her general well-being with no recurrence of symptomatic hypoglycemia, seizure, or giddiness.

  Discussion Top

Russell's viper venom is known to contain many toxins including procoagulant enzymes which activate factor V and X and other steps in the blood coagulation cascade leading to defective hemostasis. These activated coagulation proteins then accelerate coagulation reactions resulting in the formation of cross-linked fibrin and deposition of microthrombi in the microvasculature. The coagulant effect of venom is also due to an enzyme, arginine esterase hydrolase that is similar in action to thrombin, which clots fibrinogen and aggregates platelets. The proteinases in venom bring about the conversion of prothrombin to thrombin. These alterations in coagulation cascade results in the formation of microthrombi as a part of consumptive coagulopathy, the activation of fibrinolysis, and the antihemostatic effects of fibrin degradation products that lead to thrombotic and bleeding complications. It also contains a metalloproteinase 'hemmorrhagin' which damages vascular endothelium and promote vascular leakage, toxins that impair platelet function, and phospholipase A2 which has disseminated effects. [1],[3]

The various possible mechanisms proposed for the pituitary damage following snake bite include thrombosis of pituitary vessels as a part of DIC, peripheral vascular collapse followed by spasm of pituitary vessels and thrombosis of local venules leading to ischemic pituitary infarction or damaged vascular endothelium, impaired platelet function, depletion of clotting factors, and secondary fibrinolysis leading to pituitary hemorrhages. The hemorrhagic necrosis of the anterior pituitary gland was pathologically demonstrated in patients of viper bites in a study done by Proby et al. [4] Than et al., and Tun et al., who reported presence of adrenal hemorrhage apart from pituitary hemorrhages in some patients of Russell's viper bites. [5],[6] They also demonstrated presence of microthrombi and histological evidence suggestive of acute tubular necrosis in the kidneys. The AKI in our patient might be a direct consequence of DIC in addition to shock leading to prerenal failure. Normal MRI brain and absence of any focal neurological deficit in our patient ruled out the possibility of intracranial bleed due to DIC as a cause of GTCS. Her oxygen saturation and serum electrolytes were normal during seizures. Her GTCS were attributable to hypoglycemia on the basis of hypoglycemia documented in each seizure episode, symptoms and signs consistent with hypoglycemia, and resolution of those symptoms or signs including seizures after correction of hypoglycemia.

The aim of this report is to make physicians aware of the rare complication of acute pituitary failure following snake bite which requires prompt treatment with corticosteroids and/or hormone replacement therapy. When treating patients with vasculotoxic snake bites, practitioners should remain alert for recurrent hypoglycemia and/or hypotension which provide an important clue for the possibility of acute anterior hypopituitarism secondary to snake bite.

  References Top

1.David AW. Guidelines for the clinical management of snake-bites in the south-east Asia region. World Health Organization, Regional Office for South-East Asia, New Delhi; 2005. p. 1-67. http://www.toxinology.org/resources/protocols/WHO-SEARO Snakebite Guidelines 2010 copy.pdf  Back to cited text no. 1
2.Antonypillai CN, Wass JA, Warrell DA, Rajaratnam HN. Hypopituitarism following envenoming by Russell's vipers (Daboia siamensis and D. russelii) resembling Sheehan's syndrome: First case report from Sri Lanka, a review of the literature and recommendations for endocrine management. QJM 2011;104:97-108.  Back to cited text no. 2
3.Marsh NA. Snake venoms affecting the haemostatic mechanism - a consideration of their mechanisms, practical applications and biological significance. Blood Coagul Fibrinolysis 1994;5:399-410.  Back to cited text no. 3
4.Proby C, Tha-Aung, Thet-Win, Hla-Mon, Burrin JM, Joplin GF. Immediate and long-term effects on hormone levels following bites by the Burmese Russell's viper. Q J Med 1990;75:399-411.  Back to cited text no. 4
5.Than-Than, Francis N, Tin-Nu-Swe, Myint-Lwin, Tun-Pe, Soe-Soe, et al. Contribution of focal haemorrhage and microvascular fibrin deposition to fatal envenoming by Russell's viper (Vipera russelli siamensis) in Burma. Acta Trop 1989;46:23-38.  Back to cited text no. 5
6.Tun-Pe, Phillips RE, Warrell DA, Moore RA, Tin-Nu-Swe, Myint-Lwin, et al. Acute and chronic pituitary failure resembling Sheehan's syndrome following bites by Russell's viper in Burma. Lancet 1987;2:763-7.  Back to cited text no. 6


  [Table 1]


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