Case of the Month
June 2008

76-year-old male – decreased LOC

Dispatch
Your BLS and ALS units are dispatched a 76-year-old male who is said to be unconsciousness.

While en route, the dispatcher notifies you that the patient is in a private residence and has been lethargic most of the day and soaking his adult diaper(s) more than his wife of 55 years has ever seen.

En route your crew discusses the following considerations:

• Reasons for decreased level of consciousness
• Geriatric issues

Scene Size-up
Your team arrives at the scene. There is an open door to the house but no one is there. You enter and see the wife slowly moving down the hallway (holding onto the walls) as she leads you back to the patient’s bedroom. She tells you that her husband (Mr. Banner) is normally mobile with the help of a walker and despite his insulin dependant diabetes (IDD) he is typically very alert. He developed Type 2 diabetes about 25 years ago. He has been ill with vomiting and diarrhea for the past few days and has become more lethargic and weaker ever since. The pungent odor of urine is throughout the house.

Initial Assessment
You find the patient in bed lying on his back with eyes closed. His skin appears pale; he is warm and dry. When you feel his wrist for a pulse you don’t find one and immediately move to his carotid pulse where you find it present, weak and irregular at around 100/min. Respirations are deep and fast at about 30/min. A pinch of his earlobe generates minimal response. You determine he is SICK because of altered LOC, poor distal perfusion, skin signs, and his respiratory status. You confirm the location of the ALS unit.

Initial Treatment
You initiate high-percentage oxygen therapy and obtain a blood glucose reading (HIGH or 450 mg/dl). You also perform a rapid medical assessment to include breath sounds (equal and present with bilateral congestion). One of your team members is sent to bring in the gurney while vital signs are obtained.

Vital Signs

• Respirations                        30
• Pulse                                 100, irregular
• Mental status                      Very lethargic
• Pulse oximetry                     98% on NRM
• Blood sugar                         450
• Blood pressure                     86/P

Further Evaluation and Treatment
Your Lt. gets a complete history from the wife as your BLS crew prepares the patient for ALS arrival. The patient has been a diabetic for more than 25 years (Type 2) and has eye problems (diabetic retinopathy) and vascular problems in the feet (has had a few toes amputated). He has been ill for the past few days and can’t keep food down but the wife says that she is always on time with his meds to include insulin, hydrochlorothiazide [HCTZ], and atenolol for blood pressure control. Her biggest concern is the soiling of all of the adult diapers—7-10 a day for the past few days. She is very concerned by this.

The rest of the physical exam is unremarkable. The ALS unit is updated and soon arrives at the scene.  The medics initiate two large bore IVs and quickly load the patient in the back of the rig for transport. Transport is accomplished without incident.

At the hospital the patient is further evaluated and the confirmation of hyperosmolar hyperglycemic nonketotic coma (HHNC) is confirmed. The patient remains in the hospital for five days to stabilize his diabetes and treat an underlying viral infection.

Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC)
Hyperosmolar hyperglycemic nonketotic coma (HHNC) is a metabolic derangement that occurs principally in people with adult-onset diabetes. The condition is characterized by hyperglycemia, hyperosmolarity, and an absence of significant ketoacidosis. Despite the name, coma is present in fewer than 10% of cases. Most patients present with severe dehydration and focal or global neurologic deficits. In many cases, the clinical features of HHNC and diabetic ketoacidosis (DKA) overlap and are observed simultaneously.

Pathophysiology
HHNC most commonly develops in those with diabetes who have some concomitant illness that leads to a reduced fluid intake. Infection is the most common cause, but many other conditions can cause altered mentation,  dehydration, or both. Frequently, the concomitant illness is not identifiable. Hyperglycemia and hyperosmolarity lead to osmotic diuresis (frequent peeing) and an osmotic shift of fluid to the intravascular space, resulting in further intracellular dehydration.

Unlike patients with DKA, patients with HHNC do not develop ketoacidosis, but the reason for this is not known. Contributing factors probably include the availability of insulin in amounts sufficient to inhibit ketogenesis but not sufficient to prevent hyperglycemia.

History

• Most patients with HHNC have a known history of diabetes, which is usually adult onset.
• Often, a preceding illness results in several days of increasing dehydration.
• Oral hydration usually is impaired by concurrent acute illness or chronic comorbidity (e.g., dementia, immobility, vomiting).
• Severe dehydration initiates a cascade of metabolic derangements that result in progressive dehydration, hyperosmolarity, hyperglycemia, and consequent neurologic derangements.
• A wide variety of focal and global neurologic changes may be present, including the following:
• Drowsiness and lethargy
• Delirium
• Coma
• Focal or generalized seizures
• Hemiparesis

Physical
General appearance and hygiene may provide clues to the state of hydration, presence of chronic illness, and reduced level of mentation.

• Vital signs
• Tachycardia is an early indicator of dehydration; hypotension is a later sign suggestive of profound dehydration.
• Orthostatic vital signs are neither sensitive nor specific.
• Tachypnea may result from respiratory compensation for metabolic acidosis.
• Assess core temperature rectally. Abnormally high or low temperatures suggest sepsis.
• Hypoxemia can be a concurrent problem affecting mentation.

Reference for HHNC
eMedicine (external website)