CASE REPORT |
https://doi.org/10.5005/jp-journals-10089-0002 |
A Unique Case Mimicking Sepsis
1,2Department of Critical Care, Narayana Multispeciality Hospital, Ahmedabad, Gujarat, India
Corresponding Author: Anish Joshi, Department of Critical Care, Narayana Multispeciality Hospital, Ahmedabad, Gujarat, India, Phone: +91 9898539059, e-mail: dranishjoshi@gmail.com
ABSTRACT
Panhypopituitarism and adrenal crisis may mimic a case of septic shock, to begin with, and diagnosis is sometimes difficult. A definitive diagnosis is crucial for a successful outcome. Generalized weakness associated with symptoms such as drowsiness, altered sensorium, and easy fatigability are the common presentations in patients presenting to the emergency department. The symptoms may be related to the nervous system (central as well as peripheral), metabolic disorders, electrolytes, endocrinopathy, infectious diseases, toxins, trauma, etc. Early recognition with prompt management helps in preventing life-threatening complications.
We describe a case of a 50-year-old female who presented with drowsiness and generalized weakness which initially appeared as a septic shock but on detailed workup was found to be suffering from hypopituitarism. In the laboratory, the workup patient was found to be having decreased levels of pituitary hormones which were suggestive of hypopituitarism. In this case, presented here, the magnetic resonance imaging (MRI) of the brain was suggestive of "empty sella." It is a rare disorder and patients with empty sella may be asymptomatic or present with one or more pituitary hormone deficiencies. The patient was treated with hormone replacement therapy to which the patient responded well and progressively improved.
How to cite this article: Dave V, Joshi A. A Unique Case Mimicking Sepsis. J Acute Care 2022;1(1):29-31.
Source of support: Nil
Conflict of interest: None
Keywords: Empty sella, Hypopituitarism, Sepsis
INTRODUCTION
Generalized weakness is one of the common presentations of the patients presented to the emergency department and it can be related to the nervous system (central as well as peripheral), metabolic disorders, electrolyte imbalances, endocrinopathy, and infectious diseases, toxins, trauma, etc. It can be associated with other symptoms like drowsiness, altered sensorium, easy fatigability, etc.1 Sometimes reasons can be identified but many times it may remain unclear for the clinicians to identify the cause.
CASE DESCRIPTION
A 50-year female, a known case of hypothyroidism presented to the emergency room with a history of altered sensorium, drowsiness, generalized weakness, facial puffiness, and easy fatigability. On detailed history, she was found to be a drug defaulter for hypothyroidism and had hypoglycemia on presentation which was immediately corrected. She also had hypotension for which fluid boluses were given. The patient responded well to the fluid challenge. On examination, the findings were suggestive of a myxedema crisis. She was admitted to the intensive care unit (ICU) and routine investigation with ANA, thyroid profile, and anti TPO-antibody were estimated. Other organ-specific investigations were within normal limits and blood and urine cultures were negative.
Treatment was initiated with hydrocortisone 100 mg thrice daily (intravenous), oral thyroxin 400 mcg stat followed 50 mcg tapering doses of thyroxine reaching 100 mcg by day 6. Levels of follicular stimulating hormone (FSH), prolactin and cortisol levels were determined to rule out central hypopituitarism (Table 1). Diagnosis of panhypopituitarism was established and for confirmation, an MRI of the brain (pituitary) was advised, which was suggestive of “Empty Sella” (Fig. 1). On further evaluation after hormonal replacement therapy, FT4 was found in the normal range. Oral fludrocortisone 100 mg was added to the drug therapy. Later, parenteral hydrocortisone was changed to oral prednisolone 5 mg once a day. After initiation of hormone replacement therapy, the patient remained hemodynamically stable so was shifted to the room where her vitals, oxygen parameters, and urine output were monitored. Since they remained within normal limits so were discharged home and doing well on follow-up with an endocrinologist.
| Biochemistry | Patient’s values | Normal range |
|---|---|---|
| FT4 | 0.08 | 0.7–1.24 mg/dl |
| FT3 | 1.0 | 2.4–4.2 pg/mL |
| TSH | 1.22 | 0.34–4.25 mcIU/mL |
| FSH | 1.4 | 3–26 mIU/mL |
| Cortisol | 0.52 | 5–25 mcg/dl |
| Prolactin | 1.58 | 1.9–25 ng/mL |
| S. Sodium | 126 | 135–145 mEq/dl |
Fig. 1: MRI of the brain showing ‘empty’ sella; The image is suggestive of flattened hypophyseal tissue at its base, for this reason, an empty sella can be considered as herniation of the subarachnoid space into the sella turcica
DISCUSSION
In this case, the patient was a 50-year female, having reduced levels of FSH, prolactin, cortisol, and FT4 levels. A low level of FSH in a menopausal female is due to pituitary insufficiency. On the contrary, low levels of FT4/cortisol levels were suggestive of secondary thyroid insufficiency with adrenal insufficiency as well.2 The patient’s physical examination did not have any evidence of primary adrenal insufficiencies such as skin or mucosal pigmentation. MRI Brain has been done to evaluate the cause of pituitary insufficiency and it was suggestive of “empty sella.”3,4
Hypopituitarism consists of multiple deficiencies of the hormones originating from the adenohypophysis. It is divided into primary and secondary, primary disorders manifest at the pituitary level and secondary implies hypothalamic affection. Partial or complete loss of all pituitary hormones is known as panhypopituitarism.
The pituitary gland is called the “master gland of the body,” it is pea-sized and located at the center of the brain at “sella turcica”(a saddle like bony formation on the upper surface of the body of the sphenoid bone,5 containing the pituitary gland). Empty sella can be differentiated in partial empty sella syndrome (PES) where sella turcia is filled with cerebrospinal fluid (CSF) <50%, whereas incomplete empty sella syndrome (CES) where sella turcica is filled with CSF >50%. It can also be differentiated as primary and secondary empty sella syndrome. The possible causes of secondary empty sella syndrome are increased intracranial pressure because of space-occupying lesion/hydrocephalus, Sheehan’s syndrome, pituitary tumor surgery, or sequelae of cerebral radiotherapy or craniocerebral trauma. Panhypopituitarism is a condition in which the production and secretion of all of the hormones secreted from the pituitary are reduced. It is relatively an uncommon disease with high mortality. It can have a complete or partial deficiency of hormones secreted by the pituitary gland.6 The replacement of ACTH is of prime importance from all the hormones as absent or insufficient replacement is not compatible with life. There are various causes of panhypopituitarism like radiotherapy, cranial surgery, tumors, hereditary causes, infiltrative disease, infectious disease, and traumatic brain injury. Due to the underlying etiology/pathology, the clinical presentation may vary in its severity and rapidity of the onset. It can be created by very high-energy brain injury, so any symptoms associated with hormonal disorders after traumatic head injury require the evaluation of the pituitary gland (Table 2).
| Primary hypopituitarism |
|---|
| • Neoplasms causing pituitary destruction: intrasellar/parasellar/metastatic tumors |
| • Ischemic necrosis of pituitary gland: Sheehan’s syndrome, diabetes mellitus |
| • Primary empty sella syndrome |
| • Pituitary apoplexy |
| • Cavernous sinus thrombosis |
| • Iatrogenic: surgical destruction/post-radiation |
| • Aneurysm of intracranial internal carotid artery |
| • Idiopathic |
| • Infectious diseases: tuberculous meningitis/HIV/cerebral malaria |
| • Infiltrative diseases: hemochromatosis/secondary amyloidosis |
| Secondary hypopituitarism |
| • Hormone induced: glucocorticoids, gonadal hormones |
| • Traumatic brain injury |
| • Nutritional |
| • Anorexia nervosa |
| • Tumors: craniopharyngioma, germ cell tumor, lymphoma, leukemia |
| • Infectious/iatrogenic/infiltrative |
| • Severe systemic illness |
| • Psychoneuroendocrine |
| • Secondary empty sella syndrome |
The clinical manifestations of panhypopituitarism can vary from asymptomatic to subclinical to life-threatening conditions. The presentation varies depending on which hormones are involved, like the patient can present with hyponatremia/hypotension/hypoglycemia due to adrenal dysfunction so in that case, we need to rule out hypoadrenalism.7,8 Signs and symptoms may persist for years without a diagnosis. Thus, whenever there is a suspicion regarding this disease, then thorough clinical examination and diagnostic tests are the keys to reach to a diagnosis and starting the management early. Impairment of cortisol and thyroid hormones can lead to disturbances in heart rhythm and also can complicate QT prolongation (Table 3).2,9
| Hypoadrenalism |
| • Fatigability, hypoglycemia, hypotension, weakness, dizziness |
| Hypothyroidism |
| • Tiredness, weight gain, dry skin, constipation, bradycardia, slow mental status |
| Prolactin deficiency |
| • Inability to breastfeed |
| Growth hormone deficiency |
| • Decreased muscle mass, fatigue, poor quality of life |
The most important aspect of the management of panhypopituitarism after achieving the diagnosis is to supplement it with the hormones to reach its desired levels. This is stipulated as hormone replacement therapy and the patient may need to take these medications lifelong. Treatment generally differs depending on age, sex, the underlying cause of hypopituitarism, the severity of the symptoms, and the hormones involved. The management option includes (1) Hormone replacement therapy—based on which types of hormones are deficient like corticosteroids, thyroid hormones, gonadotropins, growth hormones, etc. (2) Radiation therapy—done if the cause of the damage is cancer or tumor (3) Surgical tumor removal.
CONCLUSION
Patients with septicemia can present with a variety of symptoms, but prompt evaluation and management can differentiate other rare noninfective causes. Panhypopituitarism is associated with high morbidity and mortality if not diagnosed and treated on time. Prompt hormone replacement therapy is the key and long-term follow-up is essential. Need to strategize the use of conventional radiotherapy which can limit the incidences of hypopituitarism and optimizing the treatment with long-term follow-up is mandatory.
ORCID
Vivek Dave https://orcid.org/0000-0001-9753-0793
Anish Joshi https://orcid.org/0000-0002-4754-7551
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