Hyperosmolar Coma Clinical Presentation

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

A fingerstick blood sugar measurement with a reflectance meter is the simplest first step in the evaluation. Blood sugar levels of 65-250 mg/dL exclude significant glycemic derangement and should prompt a search for other causes of MS changes. A blood sugar level outside this range 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 identifying potential causes of HNS (see Causes). Prior hospitalizations for management of hyperglycemia are important to note and indicate a patient at risk for future episodes.

HNS usually evolves over a period of days to weeks, as opposed to DKA, which develops over the course of a few days. Increasing thirst with polyuria, polydipsia, and weight loss characterize HNS. To quench their thirst, many 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.

• Clues to underlying DM

  • The presence of needle pricks or calluses on the fingertips (from home glucose monitoring) indicates glycemic derangement as the etiology of a change in MS. 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 HNS.
  • A funduscopic examination showing findings of retinopathy, premature cataracts, and xanthelasmas are also clues to underlying diabetes.
• Assessing the degree of dehydration

  • Body weight is the single most important measurement in assessing the degree of hydration. Every liter lost in body fluids results in 1 kg of loss in body weight. Unfortunately, recently recorded weights are usually not available when assessing patients with HNS, 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 MI and pulmonary emboli can be underlying etiologies of HNS. Distinguishing hypotension due to cardiac pump failure from that of severe dehydration is often difficult, especially when they coexist. Cardiac imaging or central venous pressure measurements may be required.
  • Hypotension also may be due to sepsis. Exclusion of an infectious process, especially intrathoracic, intra-abdominal, or in the soft tissues, must be included in the physical examination of patients with HNS. Document body temperature. Low-grade fever is usually present in patients with HNS, secondary to a reduction in sweating. High-grade fever suggests infection.
• Neurological examination

  • HNS may be associated with several neurological 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 neurological symptoms and signs could be the manifestation of an underlying cerebrovascular accident. Cerebral dehydration, neurotransmitter level changes in the CNS, and microvascular ischemia may contribute to these findings.
  • When HNS causes neurological dysfunction, treatment results in resolution of signs and symptoms. When neurological events lead to HNS, signs and symptoms fail to improve with correction of the metabolic derangements.

Any illness that results in dehydration or that leads to a decrease in insulin activity can precipitate HNS. Acute febrile illnesses, including infections, account for the largest proportion of HNS cases.

Complications of arteriosclerotic diseases, such as stroke, MI, and renal failure, are frequent precipitants of HNS, because of ensuing extracellular fluid changes and because of the humoral stress associated with them. Consider MI in all patients with HNS until proven otherwise.

Elevated levels of the 4 major counterregulatory hormones, whether from endogenous or exogenous sources, may precipitate HNS. Examples include acromegaly, glucocorticoid use, and elevated production of catecholamines in stress states.

Diuretics, because of the propensity toward dehydration, and any drugs capable of inducing or exacerbating insulin resistance are also potential contributors to HNS. Several medications, including beta-blockers, hydrochlorothiazide, phenytoin, encainide, cimetidine, and diazoxide, may precipitate HNS by inhibiting insulin release.

When considering treatment of a patient with HNS, identify and address acute illness and contributions from medications. Many patients with HNS do not have an underlying cause and may be treated as patients with newly diagnosed DM who presented with this syndrome.

• Conditions and illnesses associated with HNS

  • Acromegaly
  • Anesthesia
  • Burns
  • Cerebrovascular accident
  • Cushing syndrome (eg, endogenous, exogenous, ectopic)
  • Hemodialysis and peritoneal dialysis
  • GI hemorrhage
  • Heatstroke
  • Hyperalimentation/total parenteral nutrition
  • Hypothermia
  • Intestinal obstruction
  • Mesenteric thrombosis
  • Myocardial infarction
  • Neuroleptic malignant syndrome
  • Pancreatitis
  • Pneumonia
  • Pulmonary emboli
  • Renal insufficiency (chronic)
  • Rhabdomyolysis
  • Sepsis
  • Subdural hematoma
  • Surgery (especially cardiac surgery)
  • Thyrotoxicosis
  • Trauma
  • Urinary tract infection
• Medications that may precipitate HNS

  • Antiarrhythmics (eg, encainide, propranolol)
  • Antiepileptics (eg, phenytoin)
  • Antihypertensives (eg, calcium channel blockers, diazoxide)
  • Antipsychotics (eg, chlorpromazine, loxapine)^{[1, 2]}
  • L-asparaginase
  • Corticosteroids
  • Diuretics (eg, chlorthalidone, ethacrynic acid, thiazides)
  • Histamine-receptor blockers (eg, cimetidine)
  • Immunosuppressive agents