Postdengue weakness and altered sensorium

This Article


Article Information:

Group: 2010
Subgroup: Volume 8, Issue 4, Autumn
Date: September 2010
Type: Case Report
Start Page: 215
End Page: 217


  • Santosh Vastrad
  • Department of Diabetes and Endocrinology, Manipal Hospital, Bangalore, India
  • Menaka Ramprasad
  • Department of Diabetes and Endocrinology, Manipal Hospital, Bangalore, India
  • PadmaKumar ArayamParambil Vijayan
  • Medical Intensive Care Unit, Manipal Hospital, Bangalore, India
  • Arpandev Bhattacharyya
  • Department of Diabetes and Endocrinology, Manipal Hospital, Bangalore, India


      Affiliation: Department of Diabetes and Endocrinology, Manipal Hospital
      City, Province: Bangalore,
      Country: India
      Tel: +91-8025023404
      Fax: +91-8025266757


Dengue fever, also known as breakbone fever, is an acute febrile infectious disease caused by the Dengue virus belonging to the arbovirus group. We report on a patient who presented with altered sensorium, giddiness, and repeated falls after discharge from the hospital following dengue fever. The patient had hypotension on admission and hyponatremia in his initial biochemistry screen.


Implication for health policy/practice/research/medical education:
Following postdengue illness, hypopituitarism is a possibility.

Please cite this paper as:
Santosh V, Menaka R, PadmaKumar AV, Bhattacharyya A. Postdengue weakness and altered sensorium. Int J Endocriol Metab.2010;8(4):215-7.

Keywords: Postdengue fever;Weakness;Altered sensorium;Hypopituitarism

Manuscript Body:


Typical symptoms of dengue fever include febrile headache, petechial rash, and muscle and joint pains. In a small proportion of infected individuals, the disease progresses to life-threatening complications such as dengue hemorrhagic fever or shock. Falls are common symptoms in the population of patients who die from the disease, particularly among the elderly. Common causes of falls are visual, neurological, and musculoskeletal problems, with simple stumbles as the most common cause. We report a case of an elderly man whose main symptom was repeated falls 2 weeks after discharge from a mild case of Dengue fever.

Case report

A 59-year-old man was admitted in our hospital with a history of fever, body aches, and loose stools for a week. He was otherwise healthy with no significant chronic medical problems. On examination he was febrile and toxic with mild dehydration. Investigations revealed thrombocytopenia (Platlet-40,000/mm3). The rest of the baseline investigations were within normal limits including serum electrolytes. IgM and IgG antibodies for dengue antigen were positive. USG abdomen revealed mild splenomegaly. Diagnosis of seropositive dengue fever was made and treated symptomatically. He responded to the treatment well and was discharged a week after admission.
Two weeks later he presented in the emergency room with disorientation, urinary incontinence, unsteady gait, and altered sensorium. He had continued to fall for 1 week before the second admission for no apparent reason, but his wife attributed them to weakness after a serious illness and hospital stay. On examination he was pale, dehydrated, with dry, coarse skin without icterus or cyanosis. He was conscious but disoriented to time and place. A clinical examination revealed bradycardia (50/ min) and hypotension (90/60 mmHg). Systemic examination was normal. Pupils were equal and reactive to light. Baseline investigations revealed significant hyponatremia. Serum sodium was 105 mmol/L (normal 135–145). In view of hypotension and dehydration he was started on normal saline infusion and was admitted to the intensive care unit.



Figure 1. CT of abdomen showing normal adrenal gland


Figure 2. MRI Sagittal view of pituitary gland

To determine the cause of hyponatremia, a thyroid profile and cortisol test were ordered. A CT brain scan was normal. Penny dropped when his random serum cortisol report was available (4.8 mcg/dl). A second sample was collected at this point for cortisol and ACTH before starting the patient on intravenous hydrocortisone (dose of 100mg, 3 times a day). Again, his serum cortisol level (3.3 mscg/dl; normal 9–52 pg/ml) was low considering his stressful situation with low normal serum ACTH (22 pg/ml). A Synacthen test was not possible, an insulin-tolerance test was not considered given the patient’s unstable physical state. Overall, for us, pituitary functions pointed clearly to anterior hypopituitarism (TSH = 2.53 mU/ml (N = 0.3 to 5.5); FT4 = 0.39 ng/dl (N = 0.8 to 2.3); LH-1.4 mU/ml (N = 1.4 to 11); free T = 0.025 ng/ml (N = 0.28 to 11). An abdomen CT (figure1) did not reveal adrenal hemorrhage. An MRI of the pituitary gland was conducted to obtain a better visualization of the pituitary, which revealed that the gland was smaller than normal (figures 2 & 3). The patient responded well to our treatment. He was started on thyroxine (50 mcg/day), and his cortisone-replacement therapy was changed from IV to oral hydrocortisone. Additionally, he received his first injection of testosterone (serum PSA was normal and this injection was performed as a routine protocol of testosterone replacement in our unit). The patient showed remarkable improvement in his sense of well-being and daily activities.


Figure 3. MRI- Brain coronal view of pituitary gland

His blood pressure as normal as serum sodium normalized. He was discharged on thyroxine 50 mcg/ day, hydrocortisone 20 mg/day (10-5-5-0), and a monthly injection of testosterone enanthate (250 mg IM). The patient maintained normal daily activities with good biochemistry for follow up over the next 6 months. He was advised to continue the same medications with regular follow up and was also educated regarding the stressful dose of hydrocortisone.


The WHO 1997 classification divided dengue into undifferentiated fever, dengue fever, and dengue hemorrhagic fever (1). Dengue hemorrhagic fever was subdivided further into four grades (I–IV), with the two most severe being classified as dengue shock syndrome (2). The WHO's 2009 classification divided dengue fever into two groups: uncomplicated and severe. This replaces the 1997 WHO classification, which was simplified as it was found to be too restrictive, although the older classification is still widely used.
Pituitary apoplexy is defined as a clinical syndrome that may include headache, visual deficits, ophthalmoplegia, or altered mental status. It may result from either infarction or hemorrhage of the pituitary gland. Prognosis is significantly improved with early diagnosis and surgical treatment (3).  Pituitary apoplexy commonly occurs in the presence of pituitary tumor, but it can also occur in a normal pituitary gland (4). Common precipitating factors include coagulopathy, anticoagulant treatment, obstetric hemorrhage, diabetes mellitus, pituitary irradiation, and trauma. Male sex and characteristics of the adenoma  itself (especially tumor size and tumor type) rather than patient's cardiovascular risk factors, such as diabetes and hypertension, seem to predispose to pituitary apoplexy; antithrombotic therapy may also be important (5). Hypopituitarism has also been observed following aortocoronary bypass in previous case studies (6, 7).
In 1937, Sheehan concluded that pituitary necrosis was an infarction caused by ischemia rather than puerperal sepsis (8).  The pituitary gland cannot regenerate, and necrotic cells are replaced by scars. Normal pituitary function can be supported until about 50% of the gland remains intact, whereas partial or complete hypopituitarism follows the loss of 75% and 90%, respectively, of the gland. The anterior pituitary is among the most common sites of hemorrhage in hemorrhagic fever, possibly because of its localization and vascularization. The anterior pituitary receives only 10%-20% of its blood supply from superior and inferior hypophyseal arteries, whereas the remaining 80%-90% comes from hypophyseal venous portal circulation (9). A study that conducted postmortem analyses after hemorrhagic fever with renal syndrome revealed hemorrhage in 50%-100% of the sample’s cases (10). These data concur with first report of necrosis and hemorrhage in the pituitary in 60% of the fatalities in the hypotensive phase of hemorrhagic fever and in almost all who died in the oliguric phase. The atrophic changes in pituitary with consecutive hypopituitarism are similar to those described in sporadic patients. It is possible that hypopituitarism is more common than is recognized. Finally, fibrosis and pituitary atrophy can develop, resulting in hypopituitarism. A high prevalence of hypopituitarism was found in the study by Marko et al. in patients who had recovered from viral hemorrhagic fever with renal syndrome (10). It is likely that our patient developed pituitary infarct as a result of hypotension that was not so sever to develop hypocortisol crisis. Over days his Pituitary function deteriorated to the extent that he manifested with hypocortisolism and hypothyroidism. However, as expected pituitary infarction should have presented insidiously rather than subacutely which we cannot explain.
The potential for recovery following hypopituitarism is poor. Hypopituitarism is often undetected or diagnosed late, and this has severe implications on the patient’s health and sense of well-being. These findings suggest that those patients who recover from hemorrhagic fever are at high risk of developing pituitary failure as late sequelae and should be systemically investigated and treated. Particular awareness of this condition must be raised among health care workers.

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