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Hyperosmolar Hyperglycemic State Clinical Presentation

  • Author: Robin R Hemphill, MD, MPH; Chief Editor: George T Griffing, MD  more...
 
Updated: Apr 30, 2014
 

History

Most patients with hyperosmolar hyperglycemic state (HHS) have a known history of diabetes mellitus (DM), which is usually type 2. In 30-40% of cases, HHS is the patient’s initial presentation of diabetes.[3]

HHS usually develops over a course of days to weeks, unlike diabetic ketoacidosis (DKA), which develops more rapidly, over the course of a few days. Often, a preceding illness results in several days of increasing dehydration. Adequate oral hydration may be impaired by concurrent acute illness (eg, vomiting) or chronic comorbidity (eg, dementia, immobility).

Patients may complain of increasing thirst, polydipsia, polyuria, weight loss, and weakness. They do not typically report abdominal pain, a complaint that is often noted in patients with DKA.

A wide variety of 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

For patients who present with a change in mental status, obtain a rapid determination of their level of glycemia. Both hypoglycemia and decompensated hyperglycemia may manifest as mental status changes.

A blood sugar level outside the range of 65-250 mg/dL suggests an acute diabetic problem. In this case, 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.

To quench the thirst they 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. Hypoxemia can be a concurrent problem affecting mentation. The extremities may manifest evidence of peripheral volume sequestration or of dehydration.

Assessment of vital signs and body systems

Tachycardia is an early indicator of dehydration; hypotension is a later sign suggestive of profound dehydration due to volume loss secondary to osmotic diuresis. Tachypnea may result from respiratory compensation for metabolic acidosis in overlap cases.

Assess core temperature rectally. Abnormally high or low temperatures suggest sepsis as an underlying cause. Lack of fever does not rule out infection. Hypothermia is a poor prognostic factor.

Orthostatic vital signs are neither sensitive nor specific for volume status.

Perform a thorough skin examination. Skin turgor is another clue to hydration status.

Examine the head, eyes, ears, nose, and throat. Examination may reveal signs indicating altered hydration status (eg, sunken eyes or dry mouth). Cranial neuropathies, visual field losses, and nystagmus may be appreciated, which are symptoms of HHS. They are usually reversible with therapy.

HHS may be associated with several 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.

Evaluation for underlying diabetes mellitus

The presence of needle pricks or calluses on the fingertips (from home glucose monitoring) indicates glycemic derangement as the cause of a change in mental status. Similarly, ecchymoses 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.

A funduscopic examination showing findings of retinopathy, premature cataracts, and xanthelasmas are also clues suggestive of underlying DM.

Assessment of degree of dehydration

Body weight is the single most important measurement in assessing the degree of hydration. For every 1 L of body fluids lost, 1 kg of body weight is lost. Unfortunately, recently recorded weights are usually not available when patients with HHS are being assessed, and the weight reported by patients may not be accurate.

In the early stages of dehydration, cardiac stroke volume decreases. The body is able to maintain constant cardiac output by increasing the heart rate. Therefore, tachycardia is one of the earliest signs of dehydration. With ongoing volume loss, despite the compensatory tachycardia, cardiac output falls. To compensate for a drop in cardiac output, peripheral resistance increases.

With further volume loss, the mean arterial pressure can no longer be maintained by increasing the peripheral resistance. This is most apparent when the patient is sitting or standing; therefore, documentation of orthostatic changes in blood pressure and heart rate are very important in the assessment of volume status. With profound dehydration, hypotension occurs even in the supine position.

With moderate-to-severe dehydration, urine output falls because the body engages the renin-angiotensin-aldosterone system and antidiuretic hormone to preserve volume. Dryness of the mucous membranes, anhidrosis, poor skin turgor, and sunken eyes indicate significant dehydration.

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 2 coexist. Cardiac imaging or central venous pressure measurements may be required.

Hypotension also may be due to sepsis. Exclusion of an infectious process, especially one in the thorax, abdomen, or soft tissues, must be included in the physical examination of patients with HHS. Document body temperature. Low-grade fever is usually present in patients with HHS, secondary to a reduction in sweating. High-grade fever suggests infection.

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Complications

Cerebral edema

Cerebral edema is rare in HHS and is usually observed in patients much younger than the average age of 60 years. However, it may occur 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.

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. Aggressive correction of hyperglycemia and hyperosmolarity is indicated, especially in older patients.

Acute respiratory distress syndrome

Always monitor pulmonary function carefully during therapy for HHS. A drop in the partial pressure of alveolar oxygen during therapy for HHS may signal acute respiratory distress syndrome (ARDS), PE, MI, or a pneumonitis that has worsened with rehydration. ARDS may develop in association with underlying diseases, such as pancreatitis and MI.

Although the precise mechanism by which ARDS develops in persons with HHS remains unclear, a likely scenario is that rapid correction of hyperglycemia and hyperosmolarity gives rise to pulmonary edema in much the same manner as it gives rise to cerebral edema. 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.

Vascular complications

The severe dehydration of HHS leads to hypotension and hyperviscosity of the blood, both of which predispose patients to thromboembolic disease of the coronary, cerebral, pulmonary, and mesenteric beds. Disseminated intravascular coagulation (DIC) also may complicate HHS. Together, these vascular syndromes account for much of the morbidity and mortality in HHS. Low-dose subcutaneous heparin is advisable for all patients without a contraindication.

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Contributor Information and Disclosures
Author

Robin R Hemphill, MD, MPH Associate Professor, Director, Quality and Safety, Department of Emergency Medicine, Emory University School of Medicine

Robin R Hemphill, MD, MPH is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Acknowledgements

Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Program Director, Harbor-UCLA Medical Center

Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Joseph Michael Gonzalez-Campoy, MD, PhD, FACE Medical Director and CEO, Minnesota Center for Obesity, Metabolism, and Endocrinology

Joseph Michael Gonzalez-Campoy, MD, PhD, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, Association of Clinical Researchers and Educators (ACRE), and Minnesota Medical Association

Disclosure: Nothing to disclose.

George T Griffing, MD Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, InternationalSocietyfor Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Lewis S Nelson, MD, FACEP, FAACT, FACMT Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Attending Physician, Department of Emergency Medicine, Bellevue Hospital Center, New York University Medical Center and New York Harbor Healthcare System

Lewis S Nelson, MD, FACEP, FAACT, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David S Schade, MD Chief, Division of Endocrinology and Metabolism, Professor, Department of Internal Medicine, University of New Mexico School of Medicine and Health Sciences Center

David S Schade, MD is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, New Mexico Medical Society, New York Academy of Sciences, and Society for Experimental Biology and Medicine

Disclosure: Nothing to disclose.

Don S Schalch, MD Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics

Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society

Disclosure: Nothing to disclose.

Paulina B Sergot, MD Staff Physician, Department of Emergency Medicine, New York University/Bellevue Hospital Center

Paulina B Sergot, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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