Disease Process
Hyperglycemic hyperosmotic nonketotic syndrome (HHS) is a life-threatening condition that results as a complication of diabetes mellitus. Patients with type n2 diabetes mellitus account for approximately 90% to 95% of the cases (Adeyunka & Kondamudi, 2018). HHS is characterized by extreme hyperglycemia, a significant increase in serum osmolality, extreme dehydration, and an altered state of consciousness. The signs and symptoms of this condition include malaise, fever, general body weakness, tachycardia, and tachypnea. In cases where the triggering factor is a vascular condition, the patient may present with chest tightness, chest pain, palpitations, headache, and dizziness. A typical presentation of HHS is polyuria (increased urination) and polydipsia (increased thirst). Also, the patients may exhibit lethargy, a focal neurologic deficit, and a low Glasgow coma scale. In severe cases, the patient may be in a state of comatose.
This condition is precipitated by factors such as type 1 or 2 diabetes mellitus in children and adults, infectious diseases, and respiratory, genitourinary, and circulatory disorders. Nearly 60% of HHS cases have been attributed to the etiology of infection (Adeyinka & Kondamudi, 2018). It is explained by the insensible loss of water and endogenous release of catecholamines. Additionally, consuming beverages rich in carbohydrates and obese patients have been noted to increase the risk of HHS. However, this condition is on the rise in pediatric patients with type 2 diabetes.
Consequently, certain medications used in treating particular chronic ailments among the elderly with type 2 diabetes trigger this condition. These medications include; thiazide diuretics, glucocorticoids, beta-blockers, and certain atypical antipsychotics. Cardiovascular affront, like myocardial infarction, stroke, and angina pectoris, may prompt a stress response. Hence, counter-regulatory hormones are released with increased blood glucose, leading to osmotic diuresis, dehydration, and, eventually, HHS.
The pathophysiological hallmark of HHS is insulin deficiency. As a result of insufficiency of this vital hormone, glucose utilization by the peripheral tissue decreases, causing hyperglycemia. The peripheral tissues undergo “starvation.” Gluconeogenesis and glycogenolysis are then triggered by the production of counter-regulatory hormones like cortisol, glucagon, growth hormone, and catecholamines (Gosmanov & Gosmanova, 2021). As a result, the serum glucose level increase, but peripheral tissue absorption for tissue metabolism declines, thus, creating a vicious cycle. The resulting hyperglycemia considerably raises the serum osmolarity. The glucose level in HHS is typically higher than 600 mg/dL.
Furthermore, hyperglycemia causes an increase in the osmotic gradient, which makes free water be pulled out of the extravascular space. Through urine excretion, free water, electrolytes, and glucose are lost, which causes glycosuria and dehydration ranging from moderate to severe. However, ketone body production is slight in HHS compared to DKA since insulin, which hinders ketogenesis, is still produced by pancreatic beta cells.
Several diagnostic tests are used in the confirmation of HHS diagnosis. Based on the American Diabetic Association and current international guidelines, this condition is distinct by plasma osmolarity of more than 320mOsm/L, a plasma glucose level of more than 600mg/dL, and the absence of ketoacidosis. However, the first step of evaluation requires a detailed patient history and physical exam to determine the onset of the symptoms. The first laboratory test determines the serum glucose level, typically from 600 to 12000mg/dl (Gosmanov & Gosmanova, 2018). The greater the glucose level, the higher the serum osmolality and elevated degree of dehydration. Sodium, potassium, bicarbonate, magnesium, and phosphorus are also measured to determine the alterations in confirming HHS diagnosis.
Arterial blood gas plays a significant role in determining the level of acidosis. Usually, pH ranges from around 7.30. In HHS, the serum pH ranges typically from 6.8 to nearly 7.2. Additionally, in renal function tests, the BUN and creatinine levels are generally elevated in HHS. The serum enzyme levels, such as transaminases, are high due to dehydration and hemoconcentration. Significantly, a complete blood count will reveal a high white blood cell count as a response to stress or an infection, triggering HHS. Also, the hematocrit and hemoglobin levels are usually elevated than usual. A urine culture, chest X-ray, and blood culture may be necessary to determine the infection source with elevated white blood cells.
Treatment and Nursing Interventions
A multidisciplinary approach is essential in the treatment of HHS. Fluid therapy is the initial step in the management of HHS. Hydration using an isotonic fluid with electrolyte replacement is the specific intervention in managing HHS. A 15 to 20mg/kg is administered as the initial bolus then an infusion rate of 200 to 250 ml/hour is the suggested rate for managing adults (Wolfsdorf et al., 2018). However, the infusion should be administered twice the maintenance rate in pediatric patients. An isotonic fluid is significant for hydration as it helps lower the amounts of counter-regulatory hormones secreted during HHS. Fluid therapy significantly expands intravascular volume and reduces BUN, serum blood glucose, and potassium levels.
The cornerstone of managing HHS is insulin therapy. However, the infusion rate while administering insulin should be lower since severe dehydration is one of the essential pathologic processes in HHS patients. The insulin rate is lowered to 0.05 U/kg/hr. Since HHS is accompanied by depletion in potassium, replacement therapy is initiated to replace the potassium. A potassium level between 3.5to 5,5mmol/L requires administration of 40mmol/L potassium replacement in infusion solution (Wolfsdorf et al., 2018). Acutely sick patients with sepsis should be determined for an infective source. If there are clinical signs of an infection or laboratory and imaging tests suggest its existence, antibiotics are administered to counter the infection.
Additionally, HHS patients have an elevated risk of venous and arterial thromboembolism. Therefore, all patients should be treated with prophylactic low molecular weight heparin throughout hospitalization unless the drug is contraindicated. Since HHS is accompanied by hypomagnesemia and hypophosphatemia, intravenous replacement of these electrolytes should be initiated. Also, bicarbonate is indicated for clients with severe acidosis and hyperkalemia.
The nursing interventions for this patient include a thorough assessment of the precipitating factors, for instance, other diseases such as diabetes or non-compliance to medication. This will aid in obtaining baseline data that will benefit the care and patient education appropriate for managing the disease. Monitor the patient’s vital signs, blood pressure for orthostatic hypotension, respirations for acetone breath, temperature, heartbeat, and the patient’s neurologic status (Adeyinka & Kondamudi, 2018). Additionally, administer fluid therapy as indicated since the primary goal of treatment is to correct the circulatory deficit in fluid volume.
Consequently, observe the aseptic infection control techniques during invasive procedures such as catheter insertion and insertion of an intravenous line since hyperglycemia weakens the immune system e clients, predisposing patients to infections. Also, teach and encourage the patient on the need for hygiene and proper skin care to counter the infection and avoid the risk of cross spread of infections. Advice the patient on the need for adequate fluid intake to reduce infection susceptibility. Teach the patient about the condition, the average level of blood glucose, signs and symptoms, prognosis, diagnostic tests, and the appropriate medications and interventions since baseline knowledge will enable the patient to make informed decisions (Gosmanov & Gosmanova, 2021). Also, teach the patient about dietary adjustments such as limiting the intake of salt, sugar, and alcohol while increasing the intake of fruits and whole grains. Nutritional adjustment is vital in managing diabetes and reducing the risk of developing related complications.
References
Adeyinka, A., & Kondamudi, N. P. (2018). Hyperosmolar hyperglycemic non-ketotic coma. https://www.ncbi.nlm.nih.gov/books/NBK482142/
Gosmanov, A. R., Gosmanova, E. O., & Kitabchi, A. E. (2021). Hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Endotext [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK279052/
Wolfsdorf, J. I., Glaser, N., Agus, M., Fritsch, M., Hanas, R., Rewers, A., … & Codner, E. (2018). ISPAD Clinical Practice Consensus Guidelines 2018: Diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Pediatric diabetes, 19, 155-177.
write