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The statement that “Desmopressin acts like insulin and lowers glucose” is incorrect because desmopressin has no role in blood glucose regulation. Diabetes insipidus is not related to insulin deficiency or insulin resistance, and desmopressin does not influence glucose levels.

The statement that “Desmopressin increases your urinary output” is also incorrect. In diabetes insipidus, the lack of antidiuretic hormone causes the kidneys to excrete large amounts of dilute urine. Desmopressin has the opposite effect: it decreases urinary output by helping the kidneys reabsorb water, which reduces the excessive urination and thirst characteristic of this disorder.

The statement that “Desmopressin helps control high blood pressure” is inaccurate because desmopressin is not used as an antihypertensive medication. Although changes in fluid retention can influence blood pressure, desmopressin’s therapeutic purpose is not to treat hypertension but to correct the water balance problem caused by ADH deficiency.

Monitoring the client’s input and output is an important intervention, especially if the pain is related to a condition such as pancreatitis or renal involvement. However, this action does not address the client’s immediate concern of severe pain and can be completed after the client’s symptoms are stabilized.

Providing a low-carbohydrate diet is not the priority at the time of admission. Clients with severe abdominal pain are often NPO until the cause of pain is identified. Dietary orders are not urgent and do not take priority over pain control.

Weighing the client using a standing scale is not appropriate to perform first in a client experiencing severe pain. Standing with significant abdominal pain may be unsafe and uncomfortable. Weight can be obtained later once the client is stabilized and more comfortable.

A decreased lactic acid level is not associated with liver dysfunction. In fact, if the liver is impaired, lactic acid may actually increase, because the liver is responsible for converting lactate into glucose through the Cori cycle. However, lactic acid levels are not specifically tied to protein metabolism problems. Therefore, this finding would not be expected in a client whose primary metabolic issue is related to protein breakdown.

A decreased uric acid level is not an expected finding in liver dysfunction affecting protein metabolism. Uric acid is a byproduct of purine metabolism and is more closely related to kidney excretion or conditions like gout. Although liver disease can alter many metabolic pathways, uric acid levels do not reliably reflect the liver’s ability to process proteins and are not a hallmark sign of impaired hepatic protein metabolism.

An increased lactase level is incorrect because lactase is an enzyme produced in the small intestine, not the liver. Lactase levels have no relationship to liver function or protein metabolism. Lactase is involved in carbohydrate digestion, specifically the breakdown of lactose, and therefore this option is unrelated to the client's condition.

This is not an appropriate task to delegate to unlicensed assistive personnel (UAP). Checking blood glucose in an unstable situation, especially when symptoms suggest hyperglycemia from TPN, requires assessment, interpretation, and nursing judgment. Many facilities allow UAP to perform finger-stick glucose checks under routine circumstances, but in this case, the client is symptomatic and potentially unstable, so the nurse must obtain and interpret the glucose level personally.

Assessment is a nursing responsibility and cannot be delegated to UAP. Although UAP may measure vital signs in stable clients, this client is showing signs of metabolic complications from TPN (blurred vision, polyuria, dry mouth), and interpretation of vital sign changes is required. This makes it an assessment activity and therefore non-delegable.

UAP cannot perform any action that involves adjusting IV therapy or modifying infusion rates. TPN adjustments carry significant risks and require the nurse's clinical judgment. Only a licensed nurse can manage or modify TPN settings.

This is an incorrect choice because HHS primarily affects fluid balance and glucose metabolism, not oxygenation. While hypoxia can occur in some critically ill clients, most clients with HHS do not present with respiratory compromise. Administering oxygen does not correct the severe dehydration, hyperosmolarity, or electrolyte imbalances that are immediately life-threatening in HHS. Oxygen therapy may be supportive if needed, but it does not treat the core pathophysiology.

This is incorrect because the client’s serum glucose is already dangerously high, often exceeding 600 mg/dL (33 mmol/L). Giving additional carbohydrates or glucose would exacerbate hyperglycemia, worsen osmotic diuresis, and increase the risk of complications such as dehydration, electrolyte imbalance, and altered mental status. Carbohydrate intake is strictly managed after stabilization.

This is also incorrect in the acute phase because education, while important for long-term diabetes management and HHS prevention, does not address the immediate life-threatening problems. The client is typically hemodynamically unstable and may have altered mental status, making learning ineffective at this stage. Priority interventions focus on stabilizing fluid and electrolyte balance and controlling blood glucose.

Blood gases measure pH, carbon dioxide, and oxygen levels to assess acid-base balance and respiratory function. In diabetic ketoacidosis (DKA), blood gases are critical to detect metabolic acidosis. However, HHS is typically not associated with significant ketosis or acidosis. Therefore, while arterial blood gas analysis might be useful for monitoring complications such as dehydration-induced hypoperfusion or electrolyte imbalances, it does not directly confirm HHS. Relying on blood gases first could delay recognition of the primary hyperglycemic emergency.

Hypotension and orthostatic changes may be present due to dehydration from osmotic diuresis in HHS, but blood pressure alone cannot confirm the diagnosis. It is an important supportive assessment that helps gauge fluid status and perfusion, but it is secondary to identifying the hallmark hyperglycemia.

Infection is a common precipitating factor for HHS, and blood cultures may eventually be indicated to identify sepsis. However, they do not provide diagnostic confirmation of HHS. Waiting for culture results would delay treatment of the primary hyperglycemic emergency.

The antidote for acetaminophen toxicity is N-acetylcysteine, not lactulose. Lactulose does not affect drug metabolism or acetaminophen levels. This statement reflects a misunderstanding of the medication’s purpose.

Although lactulose is a synthetic sugar, its main effect is osmotic laxative action in the colon, not raising blood glucose. Using lactulose to increase glucose would be inappropriate and ineffective, particularly in a client with liver failure, who may already have metabolic disturbances.

Lactulose is commonly prescribed for clients with liver failure to prevent or treat hepatic encephalopathy. Denying its use would be misleading and incorrect.

This is incorrect as an immediate first step. While dehydration can occur in hyperglycemia, especially with hyperosmolar states or diabetic ketoacidosis (DKA), fluid administration is not the first action. The priority is identifying and correcting the cause of the extreme hyperglycemia. Fluids may be indicated after assessing the patient’s overall status and starting insulin therapy.

Removing the pump without establishing an alternative insulin delivery plan could worsen hyperglycemia. The pump is a critical source of insulin; abrupt removal without replacement could precipitate diabetic ketoacidosis (DKA).

Giving a bolus via the pump without assessing the cause of the alarm or verifying that the pump is functioning correctly may not correct the hyperglycemia. If the pump is empty or malfunctioning, the bolus would not be delivered effectively. Administering insulin without confirming the delivery method is unsafe.