Improper management of diabetic ketoacidosis

June 29, 2020

By Gracie Awalt, Marketing Associate, and
Kassie Toerner, Senior Risk Management Representative

Presentation
On December 15 at 10:23 a.m., a 12-year-old boy with a history of insulin-dependent diabetes mellitus came to an emergency department (ED) with sore throat, cough, abdominal pain, anorexia, nausea, vomiting, and diarrhea for three days. The patient’s blood sugar and hemoglobin A1c levels were elevated. The patient’s height was recorded as 5’4’’ and weight as 150 pounds.

He had a temperature of 99 degrees, heart rate of 199 bpm, respiratory rate of 18, blood pressure 98/60 mm Hg, and 100% oxygen saturation of room air. The nurse noted the patient’s breath was fruity.

Two years before, the patient was diagnosed with diabetes after coming to the ED with a 496 mg/dL blood sugar and in a state of acidosis and ketosis. Two days later, the patient was discharged after insulin infusion.

 

Physician action
Emergency Medicine Physician A ordered lab studies for the patient. Results revealed blood glucose level over 800 mg/dL and a very low venous blood gas pH of 6.8. The physician’s primary impression upon admission was diabetic ketoacidosis (DKA). The physician’s secondary impressions were abdominal pain, acute vomiting, and severe dehydration.

At 11:04 a.m., Emergency Medicine Physician A ordered a bolus of 1000 mL of sodium chloride 0.9% to be administered to the patient via IV. An additional 1000 mL at a rate of 250 mL/hr. was ordered at 11:40. At 12 p.m., another 1000 mL was ordered to be given over an hour.

Emergency Medicine Physician A admitted the patient to the ICU under the care of Pediatrician A and ordered a consultation from critical care specialist Pediatrician B and a pediatric endocrinologist.

At 12:20 p.m., Pediatrician B performed a DKA consult in the ICU. He documented his plan to monitor the patient’s hyperkalemia; continue measured rehydration; and perform an abdominal x-ray. A consult with an endocrinologist was recommended.

After admission to the ICU, Pediatrician A noted the patient was sleepy but could answer questions; had no evident gross neurological deficits; normal bowel sounds; and a non-distended and soft abdomen with mild and diffuse tenderness with no organomegaly. The patient was dehydrated with dry mucous membranes and oropharynx and showed slight erythema with moderate-sized tonsils, but no exudates in the posterior pharynx. He was experiencing moderate tachycardia; heart sounds S1 and S2 were heard with no murmurs. The patient weighed 116 pounds on a bed scale. (He had weighed 150 pounds in the ED.)

Additional IV fluids were ordered, but only one order was followed. A nurse told the pediatric endocrinologist that the patient’s blood sugar was dropping too quickly; no other orders were given.

The pediatric endocrinologist noted the patient believed the DKA was caused by acute gastroenteritis, and it was documented that DKA with Type 1 diabetes can be triggered by gastroenteritis. It was recommended the patient be observed on IV basal/bolus insulin plus IV fluids.

Two hours after admission to the ICU, the patient’s temperature rose to 100.4 degrees and heart rate to 130 bpm. Pediatrician A ordered a dose of 650 mg of acetaminophen rectal suppository to reduce the fever. Fifty minutes later, the patient had a seizure and was given lorazepam 1 mg. Soon after, the patient had an anaphylactic reaction with flushing of the face and chest and respiratory distress.

A code blue was called, and Emergency Medicine Physician B intubated the patient and administered a dose of diphenhydramine. A pediatric neurology consult was ordered to help with seizure management and complications due to severe hyperglycemia and DKA. The neurologist recommended the patient be transferred to a higher level of care. The patient was given famotidine and hydrocortisone sodium succinate to prevent further allergic symptoms.

Pediatrician B visited the patient in the ICU, and a CT of the head indicated diffuse brain swelling with open ventricles and no shift. Effacement of ventricle portions, basilar cisterns and sulci were concerning for diffuse cerebral edema. Gray-white matter differentiation was preserved. A chest x-ray indicated mild perihilar infiltrates, documented as non-specific and potentially related to bronchitis, viral pneumonia, or edema. Hypertonic saline was ordered to decrease intracranial pressure.

The patient was hypotensive despite IV fluid maintenance. Pediatrician A documented the plan to continue fluid maintenance, insulin infusion, and respiratory support until the patient was transferred. After reviewing the patient’s record, Pediatrician B noted that the cerebral edema occurred after the patient was admitted to the ICU due to severe DKA complications.

Pediatrician B noted the patient remained unresponsive. After receiving a dose of ceftriaxone, the patient was transferred at 9:35 p.m. to a large pediatric hospital.

Upon his arrival at 10:12 p.m., the patient was immediately taken for a brain CT. The results showed complete sulci and basal cisterns effacement compatible with marked cerebral edema causing herniations.

At 10:30 p.m., a critical care specialist documented that the patient’s blood sugar dropped from the 800s to 200s in a span of 6 hours at the previous medical center. The patient also had upper arm rigidity and flexion; this was believed to indicate a seizure. The patient was given lorazepam, which caused an allergic reaction and resulted in intubation.

The critical care specialist also documented that the patient’s cerebral edema was likely due to glucose overcorrection, and that the patient required vasopressors due to hemodynamic instability.

It was documented that the patient was critically ill and had increased urine output and hyponatremia, possibly due to diabetes insipidus. At 11:34 p.m., a neurosurgery resident determined that the patient presented with diffuse anoxic brain injury. Examination and imaging were consistent with brain death.

On December 16 at 12:02 p.m., the patient, who was unresponsive, was started on vasopressin. At 6:21 p.m., a neurosurgery resident noted the clinical exam also suggested brain death. Pediatrician C noted the patient developed hypotension (70/30) that required increased vasopressors. It was concluded that the brain and brainstem had ceased to function.

On December 17, the patient was declared brain dead at 11 a.m. The death certificate listed the cause of death as DKA, cerebral edema, and brain herniation. The hospital’s diagnosis at death was brain death secondary to herniation.

 

Allegations
The patient’s family filed a lawsuit against Pediatrician A, Pediatrician B, the hospital, Emergency Medicine Physician A, and the pediatric endocrinologist. It was alleged that improper management of DKA resulted in the patient’s brain herniation and death.
 


Legal implications
Two consultants for the defense reviewed the case. One consultant thought the physicians deviated from the standard of care by obtaining an incorrect weight; administering narcotics that lowered the seizure threshold and masked signs of cerebral edema; and inappropriately documenting I/O. The patient’s recovery depended on immediate transfer to a tertiary care center.

The other consultant thought the patient was at risk for cerebral edema but was unsure if the care provided caused the patient’s death.

Both consultants agreed that fluids were excessively administered, potentially contributing to cerebral edema and rapidly decreased glucose levels.

The treating pediatric endocrinologist thought the patient developed DKA because he did not take his insulin. The consultants and pediatric endocrinologist believed the patient may have survived if care had been sought earlier.  

They believed the patient’s incorrect initial weight measurement skewed fluid replacement calculations, and that early administration of mannitol could have addressed potential brain swelling. The endocrinologist thought the patient’s glucose level fell at an acceptable rate, but fluid records were unclear and I/O documentation was inaccurate.

The endocrinologist asserted that the patient’s mortality rate was 50% with a 6.84 pH level. Although it is common for DKA patients to have mild cerebral edema, literature on the topic is inconclusive around whether progression to brain herniation is related to the treatment or the disease.

The endocrinologist criticized Pediatrician B for delaying the initial assessment in the ICU. It was noted that the hospital did not have a pediatric ICU, pediatric DKA protocol, or pediatric ICU nurses, and that the treating physician gave the hospital a pediatric DKA protocol that was not implemented.

Consultants for both the plaintiff and the defense were critical of the patient’s care. These consultants thought the patient received excessive fluid and insulin that caused complications. The plaintiff’s expert thought it caused the cerebral edema, brain herniation, and eventual death. The defense expert thought the patient should have been treated using a pediatric DKA protocol. The defense thought the physicians did not understand the cause of the patient’s seizures or recognize subsequent brain herniation when elevated blood pressure was an indicator.

 

Disposition
The case was settled on behalf of Pediatrician A and Pediatrician B. The cases against the hospital, Emergency Medicine Physician A, and pediatric endocrinologist are ongoing.

 

Risk management considerations
Treatment of pediatric patients can require specialized training and protocols. At times, the need for such specialized pediatric care in non-pediatric emergency departments or hospitals can present a challenge. Effective communication, coordination of care, and complete and contemporaneous documentation remain crucial during emergency pediatric care.

The consultants were critical of the overall communication and coordination of care among the care team in this case. It is imperative that all communications that affect a medical decision be documented in the patient’s medical chart, so the information is available to other members of the care team.

The documentation of conversations or consults should also be reviewed by the care team to ensure informed decision-making. This supports continuity of care and the safety and quality of care provided to the patient. The consultants noted that the same treatment orders were made by three different physicians. It was unclear which orders were completed or if any staff members confirmed if all orders should be followed. An environment of open and direct communication among health care providers is essential to avoid duplication or omission of critical care.

Documentation was also found to be lacking in this case. Critical input and output values that are vital for the treatment of DKA were not consistently documented in the patient’s medical record. Also, hourly neurological evaluations, per DKA protocols, were not documented if they were administered. The ordering physician should review these results and document any actions or inactions on specific results and the rationale for the decision.

The incorrect weight of the patient also presented a significant challenge. Previous visit notes, laboratory and diagnostic results, vitals, nursing notes, and communications should be reviewed. Review of the patient’s medical chart provides, among other benefits, an opportunity to ensure accuracy, confirm orders have been completed, and promote continuity of care. Medical records must be comprehensive and contemporaneous for effective diagnosis and treatment.

 

Gracie Awalt can be reached at gracie-awalt@tmlt.org.

Kassie Toerner can be reached at Kassie-toerner@tmlt.org.

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