The aging patient with hyperglycemia may present in a nonketotic comatose state known as nonketotic hyperosmolar coma. This dimension of hyperglycemia is initiated or influenced by intercurrent infection, drugs, or administered osmotic loads.
The clinical presentation starts with hyperglycemia without ketoacidosis and ends with profound dehydration. This particular hyperglycemic syndrome occurs predominantly in the elderly. Podolsky estimates that 10% to 20% of the cases of severe hyperglycemia in the elderly are dehydration without ketoacidosts or nonketotic hyperosmolar coma.1 Through early recognition and treatment tailored for the individual, the nurse can help to reduce the severity of this life-threatening condition. Recognition of the syndrome in the aging client is the principle problem.
Comatose patients may be admitted to critical care units with a history of days or weeks of polyuria and increasing thirst. Physical examination reveals a profound state of dehydration and adverse neurologic signs suggestive of diffuse cortical or subcortical damage. Massive hyperglycemia without ketosis is the cardinal biochemical feature that should alert the nurse to recognize this syndrome promptly. The gravity of this disorder is always an emergency necessitating aggressive therapy and wholly compensatory nursing care. Wholly compensatory nursing care as defined by Orem describes the nurse as providing total nursing care for the patients' inabilities. Mortality principally is due to lack of recognition and inappropriate management of secondary complications. It cannot be overemphasized that even under the best circumstances, mortality rates in hyperosmolar coma are very high.
Assess for Risk Factors
Specific risk factors include age, with or without history of maturityonset diabetes, concurrent illnesses such as infections or pneumonia, and drug therapies (Dilantin, steroids, osmotic diuretics, immunosuppressive agents, and chlorthalidine). Therapeutic procedures such as dialysis, high-protein feedings, highcarbohydrate infusion loads, all of which may result in dehydration, also may be precipitating factors.
Assess for Hyperosmolar Syndrome
At the onset, symptoms of the impending hyperosmolar state are those of uncontrolled diabetes mellitus and /or a cerebral vascular accident. The typical patient is brought to the hospital in a sleepy or confused state or comatose with a history of days or weeks of polyuria and increasing thirst. As the syndrome progresses, thirst is impaired. This may be due to an alteration of the hypothalamic thirst center secondary to hyperosmolarity or hyperglycemia. The duration of these prodromal symptoms usually is longer in the hyperosmolar syndrome than in diabetic ketoacidosis, Physical assessment reveals a striking and profound dehydration, shallow respirations, and an absence of acetone on the breath.1 In addition, patients often present a variety of adverse neurologic signs, including grand mal seizures, hemiparesis, and (+) Babinski reflexes which suggest diffuse cortical or subcortical damage.
Laboratory values typically found reveal a blood sugar value mean of 1,096 with a range from 400 to 2,706 mg. Serum acetone is negative or <2. An arterial pH mean value of 7.26 with a range of 6.81 to 7.53 is common. Serum osmolarity mean is 405 with a range from 348 to 456.' Hypokalemia and hyper-hypo natremia also are common laboratory findings.
Assessment of the client begins with the identification of the cardinal signs and symptoms of diabetes, neurologic impairment, and circulatory collapse. Nursing assessment of the client with a hyperosmolar syndrome includes continuous monitoring of the hyperglycemia and dehydration, and serial estimations of plasma serum osmolarity, electrolytes, ketone bodies, urea nitrogen, glucose, arterial pH, and PcO3. Vital signs should be checked every 15 to 30 minutes. A neurologic check is performed hourly. Any change in the mental status or level of consciousness is noted and reported.
Breath sounds are auscultated for adventitious sounds such as rales and /or ronchi. If dehydration is profound, adventitious sounds may be absent initially until fluid is replaced. Respiratory excursions are observed and the patient positioned for optimum respiratory exchange.
Cardiac sounds are auscultated searching for an Ss, which is indicative of fluid overload or early congestive heart failure. A central venous pressure (CVP) line is inserted to guide fluid therapy replacement. Monitoring the electrocardiogram for changes in cardiac conductivity secondary to hypo- or hyperkalmeia should be performed noting any prolongation of the Q-T interval, depression of the S-T segment, or flattened or inverted waves. With hyperkalemia, the first change typically seen on the electrocardiogram is a change in the T wave, which becomes peaked or tented. As the potassium level rises, the P wave becomes flattened, the P-R interval prolonged, and the QRS complex widened. Hyperkalemic electrocardiographic changes correlate well with serum potassium levels.
The possibility of thro m botic complications must be kept in mind. These clients tend to develop arterial and venous thrombosis secondary to dehydration and circulatory stasis. Heparin therapy may be initiated early to prevent these complications from developing. All major pulses are palpated frequently. Changes in motor activity, color, temperature, or palpable pulsations are recorded and reported.
Urinary output is recorded hourly. Specimens are checked for sugar, acetone, and specific gravity. An accurate intake and output is of paramount importance in determining the state of fluid balance of the client.
According to Foster, the clinical feature of hyperosmolar coma is fluid volume depletion with dehydration.2 Therapy of hyperosmolar nonketotic coma is therefore directed toward (1) correction of volume depletion, (2) correction of hyperosmolality, and (3) detection and correction of an underlying precipitating cause.
The immediate intervention should be directed toward replacing the fluid deficit, as well as correcting the hyperglycemia. Unless fluids are replaced, the patient will experience altered central nervous system functioning.
Correction of Fluid Volume Deficit
Fluid replacement has attracted considerable discussion as to the type to be administered. There are no controlled studies that permit a definite statement regarding the relative advantages of hypotonie solutions. There is agreement, however, that both electrolytes and free water are required. Podolsky believes the key to adequate therapy of hyperosmolar nonketotic coma is vigorous fluid replacement with half-strength (0.45%) normal saline.1 Following confirmation of the diagnosis, two liters of hypotonie (half-strength) saline are infused very rapidly, within a two-hour period. Thereafter, one liter of hypotonie saline is administered every two hours, titrated according to the central venous pressure (CVP). The infusion solution is changed to 5% dextrose in water (D/ W) when the blood glucose has fallen to 250 mg per 100 ml of blood.1
Other physicians, G ordon and Kabadi advocate the use of isotonic saline in all patients except those with significant hypernatremia.1 This solution is used until the plasma glucose concentration falls within the 250-300 mg percent range, at which time it is replaced by isotonic glucose (5% D/ W), 2.5% D/ W, or 0.45% saline. Regardless of the type of solution used, half of the estimated water deficit is replaced in the first 12 hours, and the remainder in the next 24 hours. At least six liters and as much as 18 liters of fluid may be necessary, with nine liters being the average amount. The dangers inherent in aggressive intravenous fluid therapy, such as congestive heart failure, can be reduced by monitoring the CVP. The CVP is initially very low, reflecting profound dehydration. The rapid rate of administration of intravenous infusions can be reduced quickly if the CVP begins to rise excessively. The acceptable range for CVP limits is between 6-12 cm H2O pressure. A Swan-Ganz catheter is used to carefully monitor the pulmonary artery wedge (PAW) pressures in these patients.
Correction of Hyperglycemic
The controversy over the regimens for insulin therapy in the treatment of hyperosmolar nonketotic coma is similar to that over fluid replacement. Clients with hyperosmolar syndrome may be more sensitive to insulin than clients with ketoacidosis. There is concern that rapid drops in plasma glucose concentrations may be responsible for increased mortality during treatment. The underlying assumption for the increased mortality is vascular collapse due to the rapid shift of glucose into the cell accompanied by water transfer from the shrunken extracellular compartment.2
On the other hand, it also is clear that extreme resistance to insulin occurs. The average insulin requirement is probably about the same or slightly less in hyperosmolar coma than in ketoacidosis. It seems likely that low-dose insulin regimens are appropriate for the treatment of hyperosmolar nonketotic coma. Regular insulin, as opposed to an intermediate-acting insulin, should be used early. The recommended initial dose of regular insulin is 25-50 units intravenously. ' Regular insulin can be administered every one to two hours in the same quantity as the initial dose. If the fall in plasma glucose levels is very rapid (200-300 mg/100 ml/hr), hourly treatment with insulin should be interrupted. Additional regular insulin should not be given after the blood glucose level reaches 300 mg per 100 ml. Often, no additional insulin will be required after the initial dose. Insulin sensitivity is variable; therefore, careful tit ratio n of regular insulin is of paramount importance. Insulin should not be added to the intravenous infusion bottle because a significant amount is lost by the adherence of insulin to the bottle and tubing.
After recovery from the acute episode, the patient may need a daily dose of intermediate-acting insulin. Thereafter, clients may be without exogenous insulin. Many clients can be changed from diet plus insulin therapy to diet alone or diet plus sulfonylurea therapy.
Correction of Electrolyte Imbalance
Insulin therapy can lead to a precipitous fall in serum potassium level in these clients. Likewise, the hyperglycemia-induced osmotic diuresis causes a shift of intracellular potassium into the plasma, followed by urinary loss and depletion of body potassium. Intracellular potassium depletion invokes acute abdominal pain that may complicate the illness and often signifies a life-threatening vascular thrombosis. Podolsky states, without a doubt, that the mortality in some cases of hyperosmolar nonketotic comas has been related to potassium depletion and its adverse effects upon the myocardium and respiratory muscles.1
Potassium replacement is started earlier in the therapy of nonketotic diabetic coma than in diabetic ketoacidosis because of the greater prodromal potassium loss. Potassium depletion is the result of urinary loss and insulin therapy. Potassium replacement should be initiated early in the hypokalemic patient, provided that cardiac function is monitored and that urinary output is adequate. Once adequate urinary output is established, at least 20 to 40 mEq of potassium chloride can be added to each liter of parenterai fluid. Infusion of potassium should be stopped if serum potassium levels rise above 5.0 mEq /L. Potassium infusion should be doubled if levels fall below 4.0 mEq/ L. As much as 200-300 mEq of potassium may be required during the first 36 hours of therapy.1
Urine, blood, and sputum cultures also may be considered as part of the workup, since infection is considered to be a common precipitating factor. The search for the underlying cause is important to resolve in order to prevent recurrence of this acute condition.
In summary, the management of the hyperosmolar syndrome includes early recognition of the syndrome and prompt correction of dehydration, hyperglycemia, and hypokalemia. The nurse is instrumental in the early detection of coma and death in this life-threatening syndrome. As long as the patient has one or more of the risk factors identified earlier, the nurse should continue to monitor the patient for signs of progression of hyperosmolar nonketotic coma. If signs and symptoms of the syndrome are exhibited, an individualized treatment schedule based on sound physiologic principles should be initiated.
- 1. Podolsky S: Hyperosmolar nonketotic coma in the elderly diabetic. Med Clin North Am 1978; 4:815-825.
- 2. Foster DW: Insulin deficiency and hyperosmolar coma. Adv Intern Med 1974; 19:159-173.
- 3. Gordon EE, Kabad UM: The hyperglycémie hyperosmolar syndrome. Am J Med Sd 1976; 252-262.
- Joffe BI, et al: Pathogenesis of non-ketotic hyperosmolar diabetic coma. Lancet 1975; 1:1069-1071.