Which symptoms does the nurse observe in a client with hyperosmolar hyperglycemic syndrome?

Hypoglycemia

Inadvertent hypoglycemia is the most frequent complication of insulin therapy [22–24].

Frequency: In a review of severe hypoglycemia (requiring assistance) 11 studies of insulin-treated patients with type 2 diabetes were analysed; each included at least 50 patients followed for a minimum of 6 months [25]. The reporting of severe hypoglycemia varied enormously, from none at all to 73 episodes per 100 patient years. Prospective and retrospective studies had different reporting rates, with lower rates in prospective studies. This may have been due to the study populations, with possible exclusions in prospective studies, including those with frequent hypoglycemia or hypoglycemia unawareness. Risk factors for severe hypoglycemia in type 2 diabetes were increasing age and duration of diabetes.

Over 5% of deaths in diabetes can be attributed to hypoglycemia. The frequency increases with rigorous maintenance of normoglycemia [26,27]. In the Diabetes Control and Complications Trial (DCCT) [28] the frequency of serious hypoglycemia was more than three times increased in the intensively treated group, and the frequency of the attacks was related to the concentration of HbA1c [29]. The UK Prospective Diabetes Study in patients with type 2 diabetes also showed an increased risk of hypoglycemia with more intensive treatment [30].

In a 12-month open study of 64 patients with type 2 diabetes (mean age 58 years) who used either once-daily bedtime NPH insulin + tablets or twice-daily 30% soluble + 70% NPH, there was less hypoglycemia in the former (2.7 hypoglycemic events per person compared with 4.3); the improvement in HbA1c was similar [31]. Weight gain was also less in those who used once-daily NPH (1.3 kg compared with 4.2 kg).

The risk of hypoglycemia in intensive care has been studied retrospectively in 2272 patients. Hypoglycemia was associated with diabetes, sepsis, a Sequential Organ Failures Assessment score of 1 or more, the use of bicarbonate in renal replacement, female sex, use of vasopressors or insulin, and impaired nutrition without altered insulin dosage [32]. Various protocols have been designed and studied to try to reduce the risk of hypoglycemia when infusing insulin to maintain normoglycemia in critically ill patients [33,34].

In a review of 102 consecutive drug-induced, hospital-related cases of coma, 23 were caused by insulin only, 14 by insulin + glibenclamide, and 3 by insulin + metformin [35]. The likelihood of readmission for hypoglycemia after a previous admission was 2.9 times greater.

Of 546 Spanish diabetic children and teenagers, 14% had one period of hypoglycemia and 21% had more than one episode [36]. The highest incidence was in the morning, possibly related to the frugal Spanish breakfast and abundant food intake in the evening.

Etiology and Clinical Features

Hyperglycemic coma usually occurs in the at-risk population during severe metabolic stress, such as infections, burns, inflammatory diseases, or steroid use; it can also occur spontaneously. Table 1 summarizes some common predisposing factors of nonketotic hyperglycemia.

Table 1. Conditions causing nonketotic hyperglycemia

1.

Inappropriate insulin dosing

Serious systemic illness

Advanced dehydration

Severe acute metabolic stress (infection, inflammation, burns, myocardial infarction, Cushing's syndrome)

Surgery or anesthesia

Specific states of impaired carbohydrate tolerance (e.g., burns, drug therapy plus parenteral hyperalimentation)

Drug therapy that impairs fat mobilization in ketosis-susceptible patients (e.g., propranolol therapy)

Patients with NKH and DKA sufficiently severe to induce coma have a profoundly contracted extracellular volume with clinically undetectable jugular venous pressure. Tissue turgor is reduced and mucus membranes are dry with sunken eyeballs. Kussmaul respirations and the unmistakable fruity breath are caused by metabolic acidosis and expired acetone and are characteristic of DKA, but not NKH. The development of coma follows a predictable course starting with confusion followed by lethargy, stupor, and finally coma. In NKH, focal neurological findings may include hemiplegia, aphasia, or focal motor seizures. Hemichorea–hemiballism (HC–HB) is a movement disorder complication of NKH most commonly affecting women. Magnetic resonance imaging findings in HC–HB include reversible T1 hyperintensities and T2 hypointensities in the striatum. The pathophysiology of HC–HB is not fully understood.

Ileus

An ileus is defined as intestinal distention and the slowing or absence of passage of luminal contents without a demonstrable mechanical obstruction. An ileus can result from a number of causes, including those that are drug induced, or from metabolic, neurogenic, and infectious factors (Box 50.3).

Pharmacologic agents that can produce an ileus include anticholinergic drugs, autonomic blockers, antihistamines, and various psychotropic agents, such as haloperidol and tricyclic antidepressants. One of the more common causes of drug-induced ileus in the operative patient is the use of opiates, such as morphine or meperidine. Metabolic causes of ileus are common and include hypokalemia, hyponatremia, and hypomagnesemia. Other metabolic causes include uremia, diabetic coma, and hypoparathyroidism. Neurogenic causes of an ileus include postoperative ileus, which occurs after abdominal operations. Spinal injury, retroperitoneal irritation, and orthopedic procedures on the spine or pelvis can result in an ileus. Finally, infections can result in an ileus; common infectious causes include pneumonia, peritonitis, and generalized sepsis from a nonabdominal source.

Patients often present in a manner similar to those with a mechanical small bowel obstruction. Abdominal distention, usually without the colicky abdominal pain, is the typical and most notable finding. Nausea and vomiting may occur but may also be absent. Patients with an ileus may continue to pass flatus and diarrhea, which may help distinguish these patients from those with a mechanical small bowel obstruction.

Radiologic studies may help distinguish ileus from small bowel obstruction. Plain abdominal radiographs may reveal distended small bowel as well as large bowel loops. In cases that are difficult to differentiate from obstruction, barium studies may be beneficial.

The treatment of an ileus is entirely supportive, with nasogastric decompression and IV fluids. The most effective treatment to correct the underlying condition may be aggressive treatment of the sepsis, correction of any metabolic or electrolyte abnormalities, and discontinuation of medications that may produce an ileus. Pharmacologic agents have been used but for the most part have been ineffective. Drugs that block sympathetic input (e.g., guanethidine) or stimulate parasympathetic activity (e.g., bethanechol, neostigmine) have been tried. Hormonal manipulation, using cholecystokinin or motilin, has been evaluated, but the results have been inconsistent. Erythromycin has been ineffective, and cisapride, although apparently beneficial in stimulating gastric motility, does not appear to alter intestinal ileus. Chewing gum has been suggested as an easy and inexpensive method to stimulate the cephalic phase of digestion (e.g., vagal cholinergic stimulation and the release of gastrointestinal hormones) and therefore a potential adjunct to prevent and to treat ileus. A more recent randomized trial demonstrated that chewing gum provides no benefit regarding return of bowel function or length of stay and even suggested that postoperative ileus may be further exacerbated by the use of sugared gum.

Hyperglycaemic coma

Hyperglycaemic coma, also called diabetic coma, is the more serious of these extremes. Because the onset is gradual the patient may not be able to inform the ward staff he is not feeling well. A typical sign first noticed by the observant nurse is the patient's breathing for he may display signs of ‘air hunger’, gasping with the mouth open and showing noticeable chest movements. When approached there is a peculiar smell on his breath, an odour often described as new mown hay, which is an early indication of circulating acetone. This can be anticipated and a watch made if the patient complains of a loss of appetite, slight vomiting or abdominal pain and nausea during the preceding hours. Good nursing observation will suspect the impending signs of a developing coma, and an immediate report should be made. The suspicion can be confirmed by testing a specimen of urine taken at that time when sugar and acetone will be found. The physician may order soluble insulin to be given and glucose by mouth if possible, otherwise an intravenous infusion will be necessary. Glucose is given to prevent a rapid reversal of the hyperglycaemia when the insulin becomes active; it is at this point that the glucose balance is critical and too much insulin may cause hypoglycaemia. Because of the urgency of the situation it may be necessary to pass a catheter if a specimen of urine is not passed freely by the patient. This procedure will be ordered by the physician and should not be undertaken without his consent. The indiscriminate passing of catheters is a practice to be avoided and should only be used in an emergency, particularly where the patient's risk of sepsis is increased due to poor resistance. If necessary, the procedure must be carried out using the utmost care to reduce the chance of urinary infection.

If the patient is unconscious an intravenous infusion will be necessary as this allows continuous treatment to prevent dehydration and provides a route for administration of insulin and glucose. This is a critical period for the patient and the responsibilities of the nurse are greatly increased. Careful testing of all specimens of urine is needed, often the result of these will be a deciding factor in any variation of treatment. The hazard of caring for an unconscious patient is complicated by loss of body fluids, as this creates the possibility of the mouth becoming very dry. Frequent attention is necessary to maintain the skin and prevent pressure sores, bed bathing should be carried out at least once daily and special care is given to pressure areas at regular intervals. The patient is turned when possible to reduce pressure and friction, such movements are limited however due to the infusion which must be maintained.

It is necessary to use extra care when dealing with the mouth of an unconscious patient. Oral toilet is an important part of nursing treatment but caution is needed to prevent material used in the procedure from entering the respiratory tract The cough reflex is missing in this patient and respiratory infection will develop from inhaled substances.

When the patient regains consciousness the physician will adjust the insulin and diet to regain stability. It is important that all nurses know of such changes as the incorrect measurement of diet or insulin will result in delay to the patient's recovery. Diet received from the kitchen will be measured and prepared when sent to the ward. It is usual to send such diets in containers to eliminate mistakes, the patient's name being attached to the container. The timing of meals is important, remembering the correlation between food and insulin. The patient must eat all the food provided at each meal and if he declines to eat the full meal substitutions will be necessary.

Principles

Hypoglycemia is a common problem in patients with type 1 diabetes, especially if tight glycemic control is practiced; it is the most dangerous acute complication of diabetes. The estimated incidence of hypoglycemia in diabetic patients is 9 to 120 episodes/100 patient-years. As significant efforts continue to keep fasting and postprandial glucose concentrations within the normal range, the incidence of hypoglycemia may increase. The most common cause of coma associated with diabetes is an excess of administered insulin with respect to glucose intake. Severe hypoglycemia is usually associated with blood glucose levels below 40 to 50 mg/dL and impaired cognitive function.

Protection against hypoglycemia is normally provided by cessation of insulin release and mobilization of counterregulatory hormones, which increase hepatic glucose production and decrease glucose use. Diabetic patients using insulin are vulnerable to hypoglycemia because of insulin excess and failure of the counterregulatory system.

Hypoglycemia has many causes, such as missing a meal (decreased intake), increased energy output (exercise), and increased insulin dosage. It can also occur in the absence of any precipitant. Oral hypoglycemic agents have also been implicated in causing hypoglycemia, both during the course of therapy and as an agent of overdose.

Hypoglycemia without warning symptoms, or hypoglycemia unawareness, is a dangerous complication of type 1 diabetes and is probably caused by previous exposure to low blood glucose concentrations,14 because even a single hypoglycemic episode can reduce neurohumoral counterregulatory responses to subsequent episodes. Other factors associated with recurrent hypoglycemic attacks include overaggressive or intensified insulin therapy, longer history of diabetes, autonomic neuropathy, and decreased epinephrine secretion or sensitivity.

The Somogyi phenomenon is a common problem associated with iatrogenic hypoglycemia in the type 1 diabetic patient. The phenomenon is initiated by excessive insulin dosing, resulting in an unrecognized hypoglycemic episode that usually occurs in the early morning while the patient is sleeping. The counterregulatory hormone response produces rebound hyperglycemia, evident when the patient awakens. Often, the patient and physician interpret this hyperglycemia as an indication to increase the insulin dosage, which exacerbates the problem. Instead, the insulin dosage should be lowered or the timing changed.

Complications of Diabetes

1.

Diabetic Coma. 2 forms occur:

Keto-acidotic coma. This is common in Type 1 diabetes. Hyperosmolarity, hypovolaemia, acidosis and loss of electrolytes if unchecked lead to coma.

Hyperosmolar non-ketotic coma. This develops slowly in Type 2 diabetes. Hyperglycaemia builds up and produces profound dehydration.

Hypoglycaemic coma. This complication of treatment occurs when insulin intake is excessive for the amount of food consumed.

Cardiovascular lesions

Atheroma develops at an earlier age and with increased severity. Coronary thrombosis is common.

Microangiopathy causing occlusion of arterioles and capillaries. These vascular lesions are responsible for many of the clinical lesions e.g. cardiac failure, retinopathy, neuropathy, gangrene of limbs, Kimmelstiel–Wilson lesions in the kidney.

The frequency of cardiovascular lesions can be minimised by tight control of blood glucose levels (usually by monitoring glycated haemoglobin) and blood pressure.

Renal failure is common. It may be due to glomerulosclerosis, but pyelonephritis and renal papillary necrosis are other causes.

Infections. There is an increased susceptibility to sepsis, fungal infections and tuberculosis.

Therapeutics

Tolazamide is used as an oral hypoglycemic agent in the treatment of type 2 diabetes mellitus. As it works primarily through stimulating the secretion of insulin, it is of no use in the treatment of established type 1 diabetes, in which there is extensive autoimmune destruction of the beta-cells. Patients who are older than 40 years and have had diabetes for less than 5 years are most likely to respond. After 10 years only about 50% of patients remain satisfactorily controlled by sulfonylurea. This is referred to as secondary failure and may be attributable to beta-cell failure and/or dietary non-compliance Goldfine and Maratos-Flier (2001). There is evidence that improved control can be achieved by combining insulin with sulfonylureas Riddle and Schneider (1998).

Therapeutics

As for sulfonylurea (see therapeutics of tolbutamide), good control can be achieved with a single, daily dose.

Therapeutics

Gliquidone is used in the treatment of type 2 diabetes. As it is mostly inactivated via hepatic metabolism and excreted in the bile, with little contribution from the kidneys, it may be suitable for use in patients with renal impairmenta, in whom its pharmacokinetic appear to be little altered Harrower (1996). Gliquidone should be taken up to 30 minutes before a meal. Most patients respond to a dose of 45–60 mg given in 2–3 daily doses. (See Therapeutics of tolbutamide).

Hyperglycaemic Non-ketotic Diabetic Coma

A less common form of ‘diabetic coma’ is the hyperglycaemic non-ketotic. The aetiology and pathogenesis of the condition are not clear and suggestions only may be derived from the clinical presentation and outcome of management. Thus the presentation is often preceded by ingestion of refined carbohydrate drinks in an attempt to assuage the thirst of diabetes. Two groups are particular prone to this condition— the elderly and patients of Afro-Caribbean origin. Once the acute condition has been successfully treated, patients may be treated by diet with or without oral hypoglycaemic agents. Thus the suggestion has been made that patients presenting with hyperglycaemic non-ketotic coma have sufficient insulin circulating to inhibit lipolysis and ketogenesis but insufficient to stimulate glucose uptake into cells. The condition is diagnosed when hyperglycaemia is accompanied by a plasma osmolaelity of more than 340 mmol/kg with no significant degree of metabolic acidosis. Some degree of ketonuria may be present.

The management of hyperglycaemic non-ketotic coma is similar to that for ketoacidosis; rehydration, insulin, and electrolytes and the demands upon monitoring are therefore identical. It is worth bearing in mind that, although less common than diabetic ketoacidosis, the mortality is higher (approx. 33%).