Intern Report 7.14

Case Presentation by Luda Khait, MD

CC: “My chest hurts”

HPI: The patient is a 56yo female who presents to the emergency department as a medical code for tachycardia. She is well known to the emergency department for multiple admissions for DKA. The patient is complaining of chest pain that started earlier today, however, is unable to provide us with any more history due to confusion. She is thrashing on the stretcher, moaning, and not fully responding to questions.

ROS: Unable to obtain secondary to medical condition

Past medical history: Diabetes mellitus with multiple admissions for DKA, glaucoma, hypertension, renal insufficiency, chronic anemia
Past surgical history: Unknown
Social history: Per EMR positive history of remote drug abuse.
Family history: Diabetes
Medications: Reports she is compliant with her Insulin 70/30 10U BID, other medications unknown
Allergies: NKDA
PMD: She states she has no regular doctor

Physical Exam:
– T: 36.0 – orally
– P: 119
– BP 124/70
– R 20
– O2 sat 98% RA

GENERAL: The patient appears agitated and is hyperpnic. She is wearing clothes that appear dirty and have holes in them. She does open her eyes spontaneously, she is unable to coherently answer questions, however, is moaning in response to questions and pain.

HEENT: Head normocephalic, atraumatic Conjunctivae are pink without pallor. Pupils are 3mm bilaterally, equal, round and reactive to light.

NECK: Supple. Trachea midline.

HEART: Tachycardic rate, regular rhythm, no murmurs, rubs or gallops

LUNGS: Lungs are clear to auscultation bilaterally, no wheezes, rales, or ronchi, increased ventilation, no retractions or use of accessory muscles.

ABDOMEN: The abdomen is soft, nondistended. It is diffusely tender to palpation no rebound or peritoneal signs, no increased tenderness at McBurney’s point, negative Murphy’s sign.

EXTREMITIES: Dorsalis pedis and radial pulses are 2+ bilaterally. No pedal edema.

NEUROLOGIC: The patient is alert. Her face appears symmetric. She smiles and closes her eyes symmetrically. She responds to some commands and moving all 4 extremities with good strength and purpose. We are unable to evaluate her speech at this time, since she is moaning in response to questions.

ED Course: 
In the resuscitation bay, the patient was immediately placed on an O2/cardiac monitor, which revealed an O2 sat of 98% on room air and sinus tachycardia. Nursing staff placed two large bore peripheral IV lines and basic labs were drawn. Two boluses of NS were started wide open. Accucheck revealed a CBG >600.

A 12-lead ECG was obtained:









Chest XR revealed no pneumothorax or pulmonary infiltrates.

BMP: Na 142, K 4.7, Cl 91, HCO3 5, BUN 42, Cr 2.25 BG 1,037
AG: 46
CBC: WBC 11.4, Hgb 9.6, Hct 31.5, Pl 438
ABG: 7.15/15/126/8.1
Beta Hydroxybuterate: >100


Question 1: What is the most likely cause of this patient’s change in mental status?
A)   Hyperglycemia
B)   Dehydration
C)   Hyperosmolarity
D)   Acidosis
E)   Hyponatremia

Question 2: In the treatment of DKA, what is the ABG pH for which bicarbonate therapy is recommended?
A) pH < 6.8
B) pH < 7.0
C) pH < 7.1
D) pH < 7.3

Question 3: In a diabetic patient with refractory hypoglycemia, what medication are you most suspecting responsible for this finding?
A)   Pioglitazone
B)   Glyburide
C)   Metformin
D)   Rosiglitazone

Part B: Name a treatment for hypoglycemia associated with Type II DM (not glucose in any form).


Answers & Discussion
1) C
3) B
Bonus) Octreotide

Question 1: C. The pathophysiology of DKA involves concurrent insulin deficiency and glucagon excess that combine to produce a hyperglycemic, dehydrated, acidotic patient that has profound electrolyte abnormalities. Although all of the above can contribute to altered mental status, the most important factor is hyperosmolarity, a result of hyperglycemia and dehydration. The renal tubules begins to excrete glucose in the urine (glycosuria) when the blood glucose reaches a level above 160-180 mg/dl; the proximal renal tubules become overwhelmed at that level and are unable to resorb the excess glucose. The excess glucose in the renal tubules draws water and other electrolytes, via an osmotic effect, into the urine. This osmotic diuresis along with dehydration from poor oral intake and vomiting promotes hyperosmolarity and altered mentation. Ketoacidosis is also an important factor that can determine mentation, however, it has a contributory effect with hyperosmolarity, rather than absolute effect on its own in DKA.

The formula for serum osmolality is = 2(Na+) + Glucose/18

One must be very careful when interpreting the laboratory values in a patient with suspected DKA. The serum sodium levels are often misleadingly low in hyperglycemic states. In profound dehydration, sodium levels are usually on the lower end secondary to hyperglycemia, hypertriglyceridemia, low salt intake, increased GI/renal losses, along with perspiration/insensible losses. The pathophysiology of falsely low sodium is due to water flowing from cells into the intracellular space due to the marked hyperosmolarity, creating a dilutional hyponatremia. The true value of sodium can be calculated by adding 1.3-1.6 to the sodium lab value for every 100mg/dL of glucose above the normal value. This calculation cannot be accurately used, however, if profound hyperlipidemia is noted. Hypertriglyceridemia is a common finding in DKA, owing to the fact of impaired lipoprotein lipase activity and overproduction of hepatic VLDLs. These lipids further promote dilution of the blood and falsely decrease sodium concentrations.












Question 2: B. The use of bicarbonate therapy in treating DKA is controversial. Successful treatment of DKA involves correction of dehydration, hyperglycemia, and electrolyte imbalances. Initially, ABCs should be established. The initial fluid therapy is directed toward total intravascular volume expansion as well as restoration of renal perfusion. Typically, normal saline is used at a rate of 15-20ml/kg /hr. If the patient is in hypovolemic shock, more fluids may be necessary. If the patient has other co-morbidities, such as heart failure or CKD, it is important to monitor the patient hemodynamically so to not fluid overload the patient.

In general, insulin administration shuts of ketogenesis and in turn will correct the acidosis. Bicarbonate therapy is generally not recommended by the ADA, unless the pH is below 7. Bicarbonate therapy has not been shown to improve outcomes and has actually been shown to worsen prognosis in patients with pH ranges of 6.9-7.1, and in fact, lower pH has been shown to directly inhibit further ketogenesis via a feedback mechanism. Bicarbonate shifts the oxygen-hemoglobin dissociation curve to the right via 2,3-DPG deficiency, worsening oxygen release in tissues. Also, quickly correcting the intravascular acidosis will terminate Kussmaul respirations, allowing the CO2 to cross readily into the brain circulation across the blood-brain barrier, making CSF acidic. In addition, administration of bicarbonate will drive potassium further into the cells, making hypokalemia even more pronounced. Finally, overaggressive use of bicarbonate administration may produce alkelemia later on in the treatment course, secondary to ketones being metabolized into CO2, water, and bicarbonate.

This is a guideline and the complete clinical picture should be considered, not just a number.











Question 3: B. Hypoglycemia is a major and most dangerous complication associated with both type 1 and type 2 diabetes. Severe hypoglycemia is typically defined as blood glucose levels below 40-50mg/dL associated with altered mentation. It occurs when patients use too much insulin/oral hypoglycemic medication and either have decreased oral intake, increased energy expenditure, or increase their insulin dosage. Patients that have had multiple bouts of hypoglycemia may become immune to the warning symptoms, causing what is known as hypoglycemia unawareness. This in turn can result in significant morbidity and mortality. Since their blood sugar can plummet without their awareness, these patients may become unresponsive and unarousable very quickly and without warning. Signs and symptoms of hypoglycemia are a result of adrenergic drive of epinephrine. These signs and symptoms include sweating, nervousness, tremor, tachycardia, and altered mentation.

Pioglitazone and Rosiglitazone are within the thiazolidinedione class of oral hypoglycemics. This class of medications reverses insulin resistance of the muscle and fat cells, and also acts on hepatocytes to a lesser degree decreasing gluconeogenesis. Hypoglycemia is not a known side effect of thiazolidinediones. Glyburide, on the other hand, is a longer acting oral hypoglycemic belonging to the sulfonylurea class. This class of hypoglycemics is known to cause hypoglycemia, especially after exercise or missed meal, after being discharged from the hospital, with use of longer acting medications, and malnourished patients, amongst others. This class of medications increases insulin release from the beta cells of the pancreas at any blood glucose concentration. Metformin does not typically cause hypoglycemia because it only works when there is a baseline insulin level within the body. It acts to increase insulin’s action rather than to stimulate its release.

Patients with suspected overdose on oral hypoglycemic agents should be observed for 24 hours if hypoglycemia recurs after initial treatment in the ED. Patients that are most at risk for refractory hypoglycemia are those with impaired renal function, pediatric patients, and those patients who have just been started on an oral hypoglycemic.

In addition to frequent glucose monitoring and replacement, treatment with an agent to inhibit insulin release, like octreotide (a somatostatin analogue) canbe used. The recommended dose for adults ranges from 50-100 mcg IV or SC every 12 hours. In fact, giving patients multiple doses of D50 to raise their blood sugar in turn will stimulate more insulin to be produced, given the sulfonylureas still in the system. Although the exact mechanism of action is not known, Octreotide will block the insulin release that is caused both by the sulfonylureas and dextrose.

Prior to discharge, a meal should be given to the patient to make sure that the patient can tolerate oral feedings and this meal can begin to replenish the glycogen stores. Close outpatient follow-up is necessary to re-evaluate the oral hypoglycemic agent dose.


Conn’s Current Therapy 2014 Edward T. Bope, Rick D. Kellerman; Elsevier Inc, 2014

Rosen’s Emergency Medicine

Kitabchi A, et al. Hyperglycemia Crisis in Adult Patients with Diabetes. Diabetes Care, Volume 29, #12. December 2006.











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