Hyperosmolar Hyperglycemic State Clinical Presentation

Updated: Mar 27, 2017
  • Author: Dipa Avichal, DO; Chief Editor: George T Griffing, MD  more...
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Presentation

History

Most patients with hyperosmolar hyperglycemic state (HHS) have a known history of type 2 DM. In 30-40% of cases, HHS is the patient’s initial presentation of diabetes. [5]

HHS usually develops over a course of days to weeks, unlike diabetic ketoacidosis (DKA), which can develop in hours to a few days. Often, a preceding illness or comorbidity (eg, dementia, immobility) results in several days of increasing dehydration due to inadequate oral hydration or water loss (eg, vomiting, diarrhea).

Patients may present with polydipsia and polyuria, depending on hydration status. Other common symptoms include nausea, vomiting, weakness, lethargy, and muscle cramps. They do not typically report abdominal pain, a complaint that is often noted in patients with DKA. In more advanced HHS, presentation is more likely to be altered mental status, seizures and/or coma. Patients may also present with an underlying fever, a clue to an underlying infection. [3]

A wide variety of acute focal and global neurologic changes may be present, including the following:

  • Drowsiness and lethargy
  • Delirium
  • Coma
  • Focal or generalized seizures
  • Visual changes or disturbances
  • Hemiparesis
  • Sensory deficits

It is very important to obtain a complete history from the patient or a companion, with an emphasis on recent illnesses or other conditions leading to altered insulin requirements, lack of compliance with hypoglycemic medications (including insulin), and dietary indiscretion. Emphasize identification of potential causes of HHS. Prior hospitalizations for management of hyperglycemia are important to note and indicate a patient at risk for future episodes. [10]

To quench the thirst they may experience, many HHS patients consume beverages containing glucose, including juices and soda. Attempt to quantitate the volume ingested over the preceding 24 hours to try to estimate the degree of osmotic diuresis with which the patient is presenting.

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Physical Examination

Examine the patient for evidence of HHS, focusing on hydration status, mentation, and signs of possible underlying causes, such as a source of infection. General appearance and hygiene may provide clues to the state of hydration, the presence of chronic illness, and the level of mentation. Assessment of airway, breathing and circulation (ABC) should always be the initial step for patients presenting with hyperglycemic crisis. Assessment for volume status is very important in patients with HHS. Vitals signs and physical examination will offer important clues regarding dehydration in patients with HHS. 

Vital signs related to HHS include the following:

  • Tachycardia
  • Orthostatic decrease in blood pressure
  • Hypotension
  • Tachypnea
  • Hyperthermia, if infection is present

Physical exam findings and signs related to HHS include the following:

  • Altered mental status, confusion
  • Lethargy
  • Ill appearance
  • Dry mucous membranes
  • Sunken eyes
  • Decreased skin turgor
  • Poor capillary refill
  • Weak thread pulse
  • Anhidrosis
  • Decreased urine output
  • Coma

Evaluation for underlying diabetes mellitus

The presence of needle pricks or calluses on the fingertips (from home glucose monitoring) may indicate glycemic derangement as the cause of a change in mental status. Similarly, ecchymosis on the abdomen, thighs, and arms may be signs of insulin injection. Many patients carry cards in their wallets or purses or wear bracelets or chains with a metallic plate identifying them as having DM.

Obesity, acanthosis nigricans, diabetic dermopathy, necrobiosis on the pretibial surfaces, lower-extremity ulcerations, soft tissue infections (eg, cellulitis or carbuncles), balanitis or vulvovaginitis, thrush, gingivitis, tooth decay, and the moon face of Cushing syndrome are also associated with underlying DM and should indicate consideration of HHS.

Assessment of an underlying condition

A careful cardiovascular examination is indicated in all patients with hypotension. Both cardiac pump failure from acute myocardial infarction (MI) and pulmonary embolism (PE) can be underlying causes of HHS. Distinguishing hypotension due to cardiac pump failure from that of severe dehydration is often difficult, especially when the two coexist.

Hypotension also may be due to sepsis. Exclusion of an infectious process must be included in the physical examination of patients with HHS. Low-grade fever is usually present in patients with HHS, secondary to a reduction in sweating. High-grade fever suggests infection. Hypothermia from underlying infection is a poor prognostic indicator.

Altered mentation, cranial neuropathies, and visual field losses, which are symptoms of HHS, may be appreciated. HHS may be associated with several other neurologic findings, including seizures, hemianopsia, aphasia, paresis, a positive Babinski sign, myoclonic jerks, change in muscle tone, nystagmus, eye deviation, and gastroparesis. For many patients, these neurologic symptoms and signs could be the manifestation of an underlying cerebrovascular accident. Cerebral dehydration, neurotransmitter level changes in the central nervous system (CNS), and microvascular ischemia may contribute to these findings.

When HHS causes neurologic dysfunction, treatment results in resolution of signs and symptoms. When neurologic events cause HHS, signs and symptoms fail to improve with correction of the metabolic derangements.

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Complications

Electrolyte Abnormalities

Common complications of HHS are seen secondary to rapid correction of hyperglycemia. Patients are normally administered insulin during treatment of HHS, which may lead to hypoglycemia. Hypokalemia may also result with insulin and bicarbonate administration. It is important to frequently check electrolytes during HHS treatment [10]

Cerebral edema

Cerebral edema is a rare, but frequently fatal, complication in HHS. This occurrence is usually seen in newly diagnosed diabetic children with DKA. Cerebral edema occurs from rapid lowering of glucose levels and an ensuing rapid drop in plasma osmolarity. Brain cells, which trap osmotically active particles, preferentially absorb water and swell during rapid rehydration. Cerebral edema follows, and, given the constraints of the cranium, uncal herniation may be the cause of death in persons with HHS. [10]

Signs and symptoms of cerebral edema may progress rapidly. Signs of increased intracranial pressures include headache, decreased level of consciousness, and lethargy. As worsening brain stem herniation occurs, patients may present with seizures, papilledema, bradycardia, and respiratory arrest. 

However, death from cerebral edema due to HHS is rare, presumably because the older population that it affects has underlying cerebral atrophy. Thus, even with the edema of rehydration, the intracranial volume does not reach the critical level that causes uncal herniation. (The few fatal cases of cerebral edema in HHS were mainly patients in their 20s.) Aggressive correction of hyperglycemia and hyperosmolarity with frequent laboratory monitoring is indicated, especially in older patients.

Acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is also a rare, but potentially fatal, complication of HHS. The precise mechanism by which ARDS develops in persons with HHS remains unclear, although the thought at this time is that it is due to pulmonary pressure changes. Patients, on admission, usually present with normal lung pressures. The evolution of ARDS in HHS is thought to result from a drop in partial pressure of oxygen secondary to a reduction is osmotic colloid pressure during therapy for HHS. The pressure changes from rapid correction of hyperglycemia and hyperosmolarity lead to pulmonary edema and a decreased lung compliance. [10, 18]  To compensate for hypoxia and mild acidosis, an increase in the minute ventilation with tachypnea develops. Continuing pulmonary disease may lead to acute respiratory failure that necessitates full respiratory support, including mechanical ventilation. Always monitor pulmonary function carefully during therapy for HHS. ARDS may also develop in association with underlying diseases, such as pancreatitis and MI.

Vascular complications

The severe dehydration and contracted vascular volume associated with HHS lead to hypotension and hyperviscosity of the blood, both of which predispose patients to thromboembolic disease of the coronary, cerebral, pulmonary, and mesenteric beds. This is especially true in patients who already have atherosclerosis. Disseminated intravascular coagulation (DIC) also may complicate HHS. Low-dose subcutaneous heparin is advisable for all patients without a contraindication. With aggressive treatment in HHS, vascular complication rates can be reduced to as low as 2%. [3]

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