Hyperosmolar hyperglycemic state US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Hyperosmolar hyperglycemic state. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Hyperosmolar hyperglycemic state US Medical PG Question 1: A 62-year-old man presents to the emergency department with confusion. The patient’s wife states that her husband has become more somnolent over the past several days and now is very confused. The patient has no complaints himself, but is answering questions inappropriately. The patient has a past medical history of diabetes and hypertension. His temperature is 98.3°F (36.8°C), blood pressure is 127/85 mmHg, pulse is 138/min, respirations are 14/min, and oxygen saturation is 99% on room air. Physical exam is notable for a confused man with dry mucous membranes. Initial laboratory studies are ordered as seen below.
Serum:
Na+: 135 mEq/L
Cl-: 100 mEq/L
K+: 3.0 mEq/L
HCO3-: 23 mEq/L
BUN: 30 mg/dL
Glucose: 1,299 mg/dL
Creatinine: 1.5 mg/dL
Ca2+: 10.2 mg/dL
Which of the following is the most appropriate initial treatment for this patient?
- A. Insulin, normal saline, and potassium (Correct Answer)
- B. Normal saline and potassium
- C. Insulin and potassium
- D. Insulin
- E. Insulin and normal saline
Hyperosmolar hyperglycemic state Explanation: ***Insulin, normal saline, and potassium***
- This patient is presenting with **hyperosmolar hyperglycemic state (HHS)**, characterized by severe hyperglycemia (glucose 1299 mg/dL), dehydration (dry mucous membranes, high BUN and creatinine), and altered mental status. The initial treatment involves intravenous fluids to correct dehydration, insulin to lower blood glucose, and potassium supplementation due to potential shifts as insulin is administered.
- **Normal saline** addresses the severe dehydration, **insulin** corrects hyperglycemia, and **potassium supplementation** prevents hypokalemia, which is common during HHS treatment as glucose and potassium shift intracellularly.
*Normal saline and potassium*
- While **normal saline** and **potassium** are crucial for rehydration and electrolyte balance, omitting **insulin** would fail to address the core problem of severe hyperglycemia in HHS.
- Without insulin, blood glucose levels will remain dangerously high, leading to persistent osmotic diuresis and worsening dehydration.
*Insulin and potassium*
- Administering **insulin** without addressing the profound **dehydration** with intravenous fluids can lead to **hypovolemic shock** as insulin further drives glucose and water into cells.
- Rehydration is the priority in HHS management before or concurrent with insulin administration.
*Insulin*
- Giving only **insulin** would be detrimental, as the patient is severely dehydrated and hypokalemic (K+ 3.0 mEq/L, and will drop further with insulin).
- This approach would exacerbate dehydration and could cause life-threatening arrhythmias due to severe hypokalemia.
*Insulin and normal saline*
- While addressing hyperglycemia and dehydration, omitting **potassium supplementation** is dangerous because insulin drives potassium into cells, potentially causing severe **hypokalemia** and cardiac arrhythmias.
- The patient already has a low-normal potassium level, which will likely drop further with insulin treatment.
Hyperosmolar hyperglycemic state US Medical PG Question 2: A 30-year-old woman comes to the physician because of increased urinary frequency over the past month. She also reports having dry mouth and feeling thirsty all the time despite drinking several liters of water per day. She has not had any weight changes and her appetite is normal. She has a history of obsessive compulsive disorder treated with citalopram. She drinks 1–2 cans of beer per day. Her vital signs are within normal limits. Physical examination shows no abnormalities. Laboratory studies show:
Serum
Na+ 130 mEq/L
Glucose 110 mg/dL
Osmolality 265 mOsmol/kg
Urine
Osmolality 230 mOsmol/kg
The patient is asked to stop drinking water for 3 hours. Following water restriction, urine osmolality is measured every hour, whereas serum osmolality is measured every 2 hours. Repeated laboratory measurements show a serum osmolality of 280 mOsmol/kg and a urine osmolality of 650 mOsmol/kg. Which of the following is the most likely diagnosis?
- A. Diabetes mellitus
- B. Central diabetes insipidus
- C. Primary polydipsia (Correct Answer)
- D. Cerebral salt wasting
- E. Nephrogenic diabetes insipidus
Hyperosmolar hyperglycemic state Explanation: ***Primary polydipsia***
- The patient's initial **hyponatremia** (Na+ 130 mEq/L) and low serum osmolality (265 mOsmol/kg) with **inappropriately dilute urine** (urine osmolality 230 mOsmol/kg) in the context of excessive water intake (several liters per day) is characteristic of primary polydipsia.
- The ability to concentrate urine significantly after water restriction (urine osmolality increasing to 650 mOsmol/kg) indicates that the **kidneys can respond to ADH** and that ADH secretion is intact, ruling out diabetes insipidus.
*Diabetes mellitus*
- This condition is characterized by **elevated blood glucose levels**, which are absent in this patient (glucose 110 mg/dL is normal).
- While diabetes mellitus causes polyuria and polydipsia, the specific laboratory findings (normal glucose and ability to concentrate urine after water restriction) are inconsistent with this diagnosis.
*Central diabetes insipidus*
- Patients with central DI would have **initially dilute urine** and would **not be able to concentrate urine** significantly in response to water restriction alone.
- The patient's urine osmolality significantly increased (from 230 to 650 mOsmol/kg) after water restriction, indicating intact ADH secretion and kidney responsiveness.
*Cerebral salt wasting*
- This condition typically presents with **hyponatremia** and **dehydration**, often following brain injury or neurosurgery.
- Patients usually have elevated urinary sodium excretion and clinical signs of volume depletion (hypotension, tachycardia), which are not present in this case.
*Nephrogenic diabetes insipidus*
- In nephrogenic DI, the **kidneys do not respond to ADH**, meaning urine osmolality would remain dilute even after water restriction and exogenous ADH administration.
- The patient's ability to achieve concentrated urine (650 mOsmol/kg) after water restriction rules out this diagnosis.
Hyperosmolar hyperglycemic state US Medical PG Question 3: A 56-year-old man is seen in the hospital for a chief complaint of intense thirst and polyuria. His history is significant for recent transsphenoidal resection of a pituitary adenoma. With regard to the man's fluid balance, which of the following would be expected?
- A. Hyponatremia
- B. Increased extracellular fluid osmolarity (Correct Answer)
- C. Serum osmolarity <290 mOsm/L
- D. Elevated serum ADH
- E. Elevated blood glucose
Hyperosmolar hyperglycemic state Explanation: ***Increased extracellular fluid osmolarity***
- The symptoms of intense thirst and polyuria after pituitary surgery are classic for **diabetes insipidus (DI)**, which results from insufficient **antidiuretic hormone (ADH)**.
- Lack of ADH leads to the kidneys' inability to reabsorb water, causing excessive water loss and a consequent **increase in plasma osmolality** and extracellular fluid osmolarity as water is lost disproportionately to solutes.
*Hyponatremia*
- **Hyponatremia** (low sodium) typically occurs from over-hydration or conditions causing excess ADH, such as **syndrome of inappropriate ADH (SIADH)**.
- In DI, the primary problem is water loss leading to **hypernatremia** (high sodium) and increased osmolarity.
*Serum osmolarity <290 mOsm/L*
- Normal serum osmolarity is approximately **275-295 mOsm/L**. A value less than 290 mOsm/L suggests **hypo-osmolarity**.
- In DI, the significant water loss due to lack of ADH leads to **increased serum osmolarity**, usually above 295 mOsm/L.
*Elevated serum ADH*
- **Elevated serum ADH** would lead to increased water reabsorption in the kidneys, resulting in concentrated urine and potentially hyponatremia.
- In central diabetes insipidus, the problem is a **deficiency of ADH** secretion or action, leading to low or undetectable ADH levels.
*Elevated blood glucose*
- **Elevated blood glucose** is characteristic of **diabetes mellitus**, where polyuria and polydipsia occur due to osmotic diuresis from high glucose levels.
- This patient's history of pituitary surgery and the specific presentation points to DI, which is a disorder of **water balance** not directly related to glucose metabolism.
Hyperosmolar hyperglycemic state US Medical PG Question 4: A 27-year-old diabetic male rushes to the emergency department after finding his blood glucose level to be 492 mg/dL which is reconfirmed in the ED. He currently does not have any complaints except for a mild colicky abdominal pain. His temperature is 37°C (98.6°F), respirations are 15/min, pulse is 67/min, and blood pressure is 122/88 mm Hg. Blood is drawn for labs the result of which is given below:
Serum:
pH 7.0
pCO2 32 mm Hg
HCO3- 15.2 mEq/L
Sodium 122 mEq/L
Potassium 4.8 mEq/L
Urinalysis is positive for ketone bodies. He is admitted to the hospital and given intravenous bicarbonate and then started on an insulin drip and normal saline. 7 hours later, he is found to be confused and complaining of a severe headache. His temperature is 37°C (98.6°F), pulse is 50/min, respirations are 13/min and irregular, and blood pressure is 137/95 mm Hg. What other examination findings would be expected in this patient?
- A. Pancreatitis
- B. Pupillary constriction
- C. Hypoglycemia
- D. Peripheral edema
- E. Papilledema (Correct Answer)
Hyperosmolar hyperglycemic state Explanation: ***Papilledema***
- The patient's presentation with **confusion**, **severe headache**, **bradycardia**, **irregular respirations**, and **elevated blood pressure** (Cushing's triad) 7 hours after treatment for **diabetic ketoacidosis (DKA)** suggests increased intracranial pressure due to **cerebral edema**.
- **Papilledema** is a key ophthalmoscopic finding in significant cerebral edema, resulting from increased intracranial pressure transmitted to the optic nerve sheath.
*Pancreatitis*
- Pancreatitis can cause abdominal pain and may be associated with DKA, but the acute neurological deterioration with signs of increased intracranial pressure after initial treatment points away from pancreatitis as the primary expected finding at this stage.
- While initial mild colicky abdominal pain could suggest pancreatitis, the late-onset confusion, headache, and vital sign changes following DKA treatment are not characteristic of pancreatitis, but rather of a severe neurological complication.
*Pupillary constriction*
- **Pupillary constriction** (miosis) can be associated with opioid overdose, pontine lesions, or certain medications, but it is not a direct or expected finding in cerebral edema causing increased intracranial pressure.
- In cerebral edema, pupils are more likely to be dilated or unequal, especially if there is uncal herniation.
*Hypoglycemia*
- While **hypoglycemia** can occur with insulin therapy, leading to confusion and neurological symptoms, the patient's blood pressure is elevated and heart rate is low (bradycardia), which are not typical signs of hypoglycemia.
- Hypoglycemia usually presents with sympathetic activation (tachycardia, diaphoresis) before progressing to bradycardia in severe cases, but the associated hypertension and irregular breathing pattern are more indicative of increased intracranial pressure.
*Peripheral edema*
- **Peripheral edema** is swelling in the extremities and is generally due to fluid overload, heart failure, kidney disease, or liver disease.
- While fluid administration during DKA treatment could potentially lead to some fluid retention, it does not explain the acute neurological deterioration, headache, and vital sign changes (Cushing's triad) seen in this patient, which are far more characteristic of cerebral edema.
Hyperosmolar hyperglycemic state US Medical PG Question 5: An 8-year old boy is brought to the emergency department because he has been lethargic and has had several episodes of nausea and vomiting for the past day. He has also had increased thirst over the past two months. He has lost 5.4 kg (11.9 lbs) during this time. He is otherwise healthy and has no history of serious illness. His temperature is 37.5 °C (99.5 °F), blood pressure is 95/68 mm Hg, pulse is 110/min, and respirations are 30/min. He is somnolent and slightly confused. His mucous membranes are dry. Laboratory studies show:
Hemoglobin 16.2 g/dL
Leukocyte count 9,500/mm3
Platelet count 380,000/mm3
Serum
Na+ 130 mEq/L
K+ 5.5 mEq/L
Cl- 99 mEq/L
HCO3- 16 mEq/L
Creatinine 1.2 mg/dL
Glucose 570 mg/dL
Ketones positive
Blood gases, arterial
pH 7.25
pCO2 21 mm Hg
Which of the following is the most appropriate next step in management?
- A. Intravenous hydration with 0.45% normal saline and insulin
- B. Intravenous hydration with 5% dextrose solution and 0.45% normal saline
- C. Intravenous sodium bicarbonate
- D. Intravenous hydration with 0.9% normal saline and insulin (Correct Answer)
- E. Intravenous hydration with 0.9% normal saline and potassium chloride
Hyperosmolar hyperglycemic state Explanation: ***Intravenous hydration with 0.9% normal saline and insulin***
- This patient presents with **diabetic ketoacidosis (DKA)**, characterized by hyperglycemia (glucose 570 mg/dL), metabolic acidosis (pH 7.25, HCO3- 16 mEq/L, ketones positive), and dehydration (dry mucous membranes, increased thirst, weight loss).
- Initial management of DKA involves aggressive **volume expansion** with **0.9% normal saline** to restore perfusion and reduce hyperglycemia; subsequently, **insulin infusion** is started to correct hyperglycemia and halt ketogenesis.
*Intravenous hydration with 0.45% normal saline and insulin*
- While insulin is crucial, **0.45% normal saline (hypotonic saline)** is generally not the initial fluid of choice for DKA due to the risk of exacerbating cerebral edema, especially in children.
- **Isotonic saline (0.9% normal saline)** is preferred for initial resuscitation to rapidly restore extracellular fluid volume.
*Intravenous hydration with 5% dextrose solution and 0.45% normal saline*
- **5% dextrose solution** should only be added to intravenous fluids when the blood glucose level falls to around 200-250 mg/dL, to prevent hypoglycemia while continuing insulin to resolve ketosis.
- Administering dextrose initially would worsen the existing severe hyperglycemia.
*Intravenous sodium bicarbonate*
- **Sodium bicarbonate** is generally not recommended for mild to moderate DKA due to potential risks like cerebral edema and metabolic alkalosis, and potential paradoxical worsening of CNS acidosis.
- Bicarbonate therapy is reserved for **severe acidosis (pH < 6.9 or 7.0)** with hemodynamic instability or impaired cardiac contractility, which is not the case here.
*Intravenous hydration with 0.9% normal saline and potassium chloride*
- While **0.9% normal saline** is appropriate, this option lacks **insulin therapy**, which is essential for treating DKA by halting ketogenesis and correcting hyperglycemia.
- Although potassium supplementation will be necessary during DKA treatment (as insulin drives K+ into cells and can cause hypokalemia), the most appropriate **next step** is to initiate both fluid resuscitation and insulin therapy together.
- The patient's current potassium level of 5.5 mEq/L is at the upper limit of normal, but reflects total body potassium depletion; potassium should be added to maintenance fluids once adequate urine output is established.
Hyperosmolar hyperglycemic state US Medical PG Question 6: A 47-year-old man is brought to the emergency department by his wife 30 minutes after the onset of nausea, sweating, and palpitations. On the way to the hospital, he had an episode of non-bloody vomiting and intravenous fluid resuscitation has been started. He has no history of similar symptoms. For the past 2 weeks, he has been trying to lose weight and has adjusted his diet and activity level. He eats a low-carb diet and runs 3 times a week for exercise; he came home from a training session 3 hours ago. He was diagnosed with type 2 diabetes mellitus 2 years ago that is controlled with basal insulin and metformin. He appears anxious. His pulse is 105/min and blood pressure is 118/78 mm Hg. He is confused and oriented only to person. Examination shows diaphoresis and pallor. A fingerstick blood glucose concentration is 35 mg/dL. Shortly after, the patient loses consciousness and starts shaking. Which of the following is the most appropriate next step in management?
- A. Administer intravenous dextrose (Correct Answer)
- B. Administer intravenous phenoxybenzamine
- C. Obtain an EEG
- D. Administer intravenous lorazepam
- E. Administer intramuscular glucagon
Hyperosmolar hyperglycemic state Explanation: ***Administer intravenous dextrose***
- The patient presents with severe **hypoglycemia** (fingerstick glucose 35 mg/dL) and associated neurological symptoms like confusion, disorientation, loss of consciousness, and seizures. **Intravenous dextrose** is the most rapid and effective treatment for severe hypoglycemia in a hospital setting.
- Due to the rapid progression of symptoms, including loss of consciousness and shaking (suggesting a seizure), immediate administration of intravenous dextrose is critical to prevent further neurological damage.
*Administer intravenous phenoxybenzamine*
- **Phenoxybenzamine** is an alpha-blocker used to manage **pheochromocytoma**, a condition that can cause symptoms like palpitations, sweating, and hypertension but usually not severe hypoglycemia.
- While pheochromocytoma can present with some similar symptoms, the patient's low blood glucose level clearly points to hypoglycemia as the primary acute issue, making phenoxybenzamine an inappropriate immediate treatment.
*Obtain an EEG*
- An **EEG (electroencephalogram)** is used to assess brain activity and diagnose seizure disorders or other neurological conditions. While the patient is seizing, the underlying cause is clearly identified as **hypoglycemia**.
- Obtaining an EEG would delay critical treatment for hypoglycemia and is not the appropriate first step in a patient with an acutely reversible metabolic cause for seizures.
*Administer intravenous lorazepam*
- **Intravenous lorazepam** is a benzodiazepine used to treat acute seizures. While the patient is seizing, the cause of the seizure is severe hypoglycemia.
- Treating the underlying hypoglycemia with dextrose will stop the seizure, making lorazepam unnecessary as the primary treatment unless the seizure persists after glucose correction.
*Administer intramuscular glucagon*
- **Intramuscular glucagon** is an appropriate treatment for severe hypoglycemia, particularly in an outpatient setting or when intravenous access is not immediately available.
- However, in a hospital setting with established IV access, **intravenous dextrose** is the preferred and more rapid method to deliver glucose directly into the bloodstream for immediate effect.
Hyperosmolar hyperglycemic state US Medical PG Question 7: A 78-year-old male with history of coronary artery disease, status post coronary stent placement currently on aspirin and clopidogrel was found down in his bathroom by his wife. His GCS score was 3 and an accurate physical exam is limited. A stat non-contrast CT scan of his brain demonstrated a large right parietal intracranial hemorrhage with surrounding edema. He was promptly transferred to the intensive care unit (ICU) for monitoring. Over the next day, his mental status continues to worsen but repeat CT scan shows no new bleeding. In addition, the patient’s urinary output has been >200 cc/hr over the last several hours and increasing. His temperature is 99.0 deg F (37.2 deg C), blood pressure is 125/72 mmHg, pulse is 87/min, and respirations are 13/min. Which of the following values would most likely correspond to the patient’s urine specific gravity, urine osmolality, plasma osmolality, and serum sodium?
- A. Low, High, High, High
- B. Low, Low, High, High (Correct Answer)
- C. High, High, Low, Low
- D. Low, Low, High, Low
- E. High, Low, Low, High
Hyperosmolar hyperglycemic state Explanation: ***Low, Low, High, High***
- This patient's presentation, particularly the **large intracranial hemorrhage**, worsening mental status despite no new bleeding, and especially the **high urinary output (>200 cc/hr)**, is classic for **diabetes insipidus (DI)**, often neurogenic DI, due to damage to the posterior pituitary or hypothalamus.
- In DI, there is a deficiency of **ADH (vasopressin)**, leading to the kidneys' inability to reabsorb water. This results in the excretion of large volumes of **dilute urine** (low urine specific gravity, low urine osmolality) and concentration of the plasma (high plasma osmolality and hypernatremia, which means high serum sodium).
*Low, High, High, High*
- This pattern would indicate concentrated urine alongside concentrated plasma and high sodium, which contradicts the presence of **polyuria** and the underlying pathology of **diabetes insipidus (DI)**.
- High urine osmolality and specific gravity would suggest intact ADH function and water reabsorption in the kidneys, which is not what occurs in DI.
*High, High, Low, Low*
- This profile describes a state of **concentrated urine** but **dilute plasma** and **hyponatremia**, which is characteristic of the **Syndrome of Inappropriate Antidiuretic Hormone (SIADH)**.
- SIADH is the opposite of diabetes insipidus, involving excessive ADH leading to water retention, not excessive water excretion.
*Low, Low, High, Low*
- While **low urine specific gravity** and **low urine osmolality** are consistent with diabetes insipidus, a **low serum sodium** (hyponatremia) is not.
- In diabetes insipidus, the loss of free water typically leads to **hypernatremia** as the body becomes dehydrated.
*High, Low, Low, High*
- This combination is inconsistent with any common clinical scenario. A **high urine specific gravity** with a **low urine osmolality** is contradictory, as specific gravity is a measure of urine concentration, which correlates with osmolality.
- Furthermore, a **low plasma osmolality** with a **high serum sodium** is physiologically improbable.
Hyperosmolar hyperglycemic state US Medical PG Question 8: A 71-year-old male presents to the emergency department after having a generalized tonic-clonic seizure. His son reports that he does not have a history of seizures but has had increasing confusion and weakness over the last several weeks. An electrolyte panel reveals a sodium level of 120 mEq/L and a serum osmolality of 248 mOsm/kg. His urine is found to have a high urine osmolality. His temperature is 37° C (98.6° F), respirations are 15/min, pulse is 67/min, and blood pressure is 122/88 mm Hg. On examination he is disoriented, his pupils are round and reactive to light and accommodation and his mucous membranes are moist. His heart has a regular rhythm without murmurs, his lungs are clear to auscultation bilaterally, the abdomen is soft, and his extremities have no edema but his muscular strength is 3/5 bilaterally. There is hyporeflexia of all four extremities. What is the most likely cause of his symptoms?
- A. Hereditary diabetes insipidus
- B. Sheehan’s syndrome
- C. Syndrome of Inappropriate Antidiuretic Hormone (SIADH) (Correct Answer)
- D. Diabetic ketoacidosis
- E. Lithium use
Hyperosmolar hyperglycemic state Explanation: ***Syndrome of Inappropriate Antidiuretic Hormone (SIADH)***
- This patient presents with **hypotonic hyponatremia** (serum Na 120 mEq/L, osmolality 248 mOsm/kg) in the setting of a **high urine osmolality**, indicating the kidney is inappropriately concentrating urine despite low plasma osmolality.
- The symptoms of **confusion, weakness, generalized tonic-clonic seizure**, and **hyporeflexia** are consistent with severe hyponatremia affecting neurological function.
*Hereditary diabetes insipidus*
- This condition is characterized by the inability to concentrate urine, leading to **polyuria** and **polydipsia**, and often hypernatremia, which is the opposite of this patient's presentation.
- Patients typically have **low urine osmolality** and high serum osmolality due to excessive water loss.
*Sheehan's syndrome*
- This syndrome is a cause of **hypopituitarism** due to postpartum hemorrhage, leading to deficiencies in various pituitary hormones, including ADH if the posterior pituitary is affected.
- ADH deficiency would lead to **diabetes insipidus-like symptoms** (high serum osmolality, low urine osmolality, polyuria) and not the hyponatremia seen in this patient unless there's profound adrenal insufficiency (cortisol deficiency), but the primary lab findings contradict ADH excess.
*Diabetic ketoacidosis*
- This condition is characterized by **hyperglycemia**, metabolic acidosis, and ketonemia, often leading to polyuria and polydipsia, and can cause **hypernatremia** or pseudohyponatremia.
- The patient's blood pressure, heart rate, and lack of symptoms like Kussmaul respirations or fruity breath do not support DKA, and his sodium is low, not high.
*Lithium use*
- Chronic lithium use can cause **nephrogenic diabetes insipidus** by interfering with ADH action in the renal tubules, leading to an inability to concentrate urine.
- This would result in **polyuria, polydipsia**, and potentially hypernatremia and low urine osmolality, which is inconsistent with the patient's findings of hyponatremia and high urine osmolality.
Hyperosmolar hyperglycemic state US Medical PG Question 9: An 18-year-old man is brought to the emergency department due to the confusion that started earlier in the day. His parents report that the patient had recovered from vomiting and diarrhea 3 days ago without medical intervention. They mention that although nausea and vomiting have resolved, the patient continued to have diffuse abdominal pain and decreased appetite. Past medical history is unremarkable, except for a recent weight loss and increased thirst. The patient does not use tobacco products or alcohol. He is not sexually active and does not use illicit drugs. He appears lethargic but responds to questions. His mucous membranes appear dry. Temperature is 36.9°C (98.4°F), blood pressure is 105/60 mm Hg, pulse is 110/min, and respiratory rate is 27/min with deep and rapid respiration. There is diffuse abdominal tenderness without guarding, rebound tenderness or rigidity. Which of the following is the next best step in the management of this patient?
- A. Abdominal ultrasound
- B. ECG
- C. MRI of the brain
- D. Capillary blood glucose measurement (Correct Answer)
- E. CT of the abdomen
Hyperosmolar hyperglycemic state Explanation: ***Capillary blood glucose measurement***
- The patient's symptoms, including **confusion**, recent **weight loss**, **increased thirst**, **lethargy**, dry mucous membranes, **tachycardia**, and **Kussmaul respirations** (deep and rapid breathing), are highly suggestive of **diabetic ketoacidosis (DKA)**.
- A rapid assessment of **blood glucose** is crucial for confirming DKA and initiating prompt treatment.
*Abdominal ultrasound*
- While the patient has **diffuse abdominal tenderness**, there are no signs pointing specifically to an intra-abdominal pathology requiring immediate imaging.
- The patient's systemic symptoms and Kussmaul respirations are more indicative of a metabolic derangement than a localized abdominal issue.
*ECG*
- An ECG might be performed later to assess for **cardiac abnormalities** in DKA, especially related to **electrolyte disturbances**, but it's not the immediate diagnostic step.
- The priority is to confirm and begin treatment for the metabolic crisis.
*MRI of the brain*
- Given the patient's acute confusion and other systemic symptoms, an MRI of the brain is not the initial investigation.
- **Cerebral edema** can be a complication of DKA, but it typically develops later in the course or during treatment, and initial management focuses on correcting the metabolic state.
*CT of the abdomen*
- Similar to abdominal ultrasound, a CT scan of the abdomen is not the next best step given the clinical picture.
- The symptoms are more consistent with a **metabolic emergency** like DKA, which requires immediate biochemical assessment rather than imaging for abdominal pain.
Hyperosmolar hyperglycemic state US Medical PG Question 10: A 72-year-old man presents to the emergency department for a change in his behavior. The patient's wife called 911 and he was brought in by emergency medical services. She noticed that he seemed somnolent and not very responsive. The patient has a past medical history of type II diabetes, obesity, osteoarthritis, and migraine headaches. His current medications include naproxen, insulin, atorvastatin, metformin, ibuprofen, omeprazole, and fish oil. His temperature is 99.5°F (37.5°C), blood pressure is 170/115 mmHg, pulse is 80/min, respirations are 19/min, and oxygen saturation is 98% on room air. On physical exam, the patient is somnolent and has a Glasgow Coma Scale of 11. Cardiac and pulmonary exams are notable for bibasilar crackles and a systolic murmur that radiates to the carotids. Neurological exam is deferred due to the patient's condition. Laboratory values are shown below.
Hemoglobin: 12 g/dL
Hematocrit: 36%
Leukocyte count: 9,500 cells/mm^3 with normal differential
Platelet count: 199,000/mm^3
Serum:
Na+: 144 mEq/L
Cl-: 98 mEq/L
K+: 4.0 mEq/L
HCO3-: 16 mEq/L
BUN: 44 mg/dL
Glucose: 202 mg/dL
Creatinine: 2.7 mg/dL
Ca2+: 9.2 mg/dL
AST: 12 U/L
ALT: 22 U/L
The patient is started on IV fluids. Which of the following represents the best next step in management?
- A. Bicarbonate
- B. Potassium
- C. Insulin and potassium (Correct Answer)
- D. Insulin
- E. Discontinue the patient's home medications
Hyperosmolar hyperglycemic state Explanation: ***Insulin and potassium***
- The patient presents with **hyperglycemia** (glucose 202 mg/dL), a **high anion gap metabolic acidosis** (anion gap = 144 - (98 + 16) = 30), and altered mental status, consistent with **diabetic ketoacidosis (DKA)** in a patient with type 2 diabetes.
- **Insulin therapy** is essential to halt ketogenesis, correct hyperglycemia, and reverse metabolic acidosis.
- **Potassium replacement** must be initiated simultaneously when serum K+ is between 3.3-5.2 mEq/L (patient's K+ is 4.0 mEq/L). Insulin drives potassium intracellularly, and without replacement, **life-threatening hypokalemia** can develop rapidly.
- Current **DKA management guidelines** recommend starting both insulin and potassium together when potassium is in the normal range to prevent cardiac arrhythmias from hypokalemia.
*Insulin*
- While insulin is critical for DKA management, giving insulin **without potassium replacement** when K+ is normal risks precipitating **severe hypokalemia** as insulin shifts potassium into cells.
- Hypokalemia can lead to cardiac arrhythmias, muscle weakness, and respiratory failure.
- Modern protocols emphasize **concurrent potassium administration** with insulin therapy.
*Bicarbonate*
- Bicarbonate therapy is **not routinely recommended** in DKA management and is reserved only for severe acidosis with pH <6.9 to prevent cardiovascular collapse.
- The patient's acidosis (HCO3- 16 mEq/L) will correct with insulin therapy as ketone production ceases.
- Bicarbonate can cause complications including **cerebral edema, paradoxical CNS acidosis, hypokalemia**, and rebound alkalosis.
*Potassium*
- While potassium replacement is necessary, it must be given **with insulin**, not alone.
- Potassium monotherapy would not address the underlying hyperglycemia and ongoing ketoacidosis.
- The patient's current potassium is normal (4.0 mEq/L), making isolated potassium therapy unnecessary without insulin.
*Discontinue the patient's home medications*
- The patient is taking multiple **NSAIDs** (naproxen and ibuprofen) that likely contributed to his **acute kidney injury** (Cr 2.7 mg/dL).
- While discontinuing nephrotoxic medications is important, this does not address the **immediate life-threatening metabolic crisis** of DKA.
- The priority is correcting the acidosis and hyperglycemia; medication reconciliation can occur after stabilization.
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