When There Are Acute Changes In Mental Status In Patients With Diabetes

Adam Lang, BS, and Kathleen Satterfield, DPM, FACFAOM

   In addition to monitoring electrolytes, one can check dehydration by ordering the following labs: total serum protein, amylase, creatinine phosphokinase and albumin.4 All will most likely be elevated with DKA. Creatinine will most likely be falsely elevated due to blood acetoacetate levels as Assadi and colleagues demonstrated.11 Leukocytosis is generally present in DKA proportional to the serum ketone concentration with values >25,000 usually indicating infection.7

What About Lactic Acidosis Or Hyperglycemic Hypersmolar Syndrome?

   Lactic acidosis. This is another cause of a high anion gap acidosis and will mimic DKA symptomology.7 A recent nested case-control analysis concentrated on 50,048 patients with type 2 diabetes. Authors revealed that metformin and sulfonylurea use have been linked to lactic acidosis in rare instances. Sulfonylureas are more likely to produce a profound hypoglycemia.12 Accordingly, one may want to inquire about diabetes medication use as it may be a factor in the differential. Other common causes of lactic acidosis include drug toxicity of salicylate, methanol, ethylene glycol and paraldehyde, as well as chronic renal failure.7

   Hyperglycemic hyperosmolar syndrome (HHS). One should always concurrently consider HHS as a differential diagnosis with DKA in the diabetic patient with an AMS.3,4,7 Hyperglycemic hypersmolar syndrome is very similar to DKA but usually develops over days to weeks rather than acutely over 24 hours.4

   Polyuria, polydipsia and fever from underlying infections do occur. There is also a significant alteration (or decline) in mental status, which is often the most outstanding presentation. Abdominal pains, vomiting, nausea and Kussmaul’s respirations generally do not occur.4 Stroke-like symptoms often occur as well. These include focal epileptic seizures and focal neurological defects (hemiparesis, hemiplegia, increased muscle tone, stroke or meningitis-like symptoms).13,14

   Infections such as UTIs and pneumonia are usually the underlying causes of HHS.4 Myocardial infarction, stroke, thyrotoxicosis and even hyperthyroid Grave’s disease can promote the release of counterregulatory hormones leading to hyperglycemia and hyperosmolarity.4,15

Significant laboratory findings for HHS include:

   • Plasma glucose >600
   • Arterial pH >7.30
   • Serum bicarbonate (mEq/L) >15
   • Effective serum osmolality > 320 mOsm/kg
   • Anion gap

Could Sepsis Be A Possible Diagnosis?

   Sepsis. The patient in this case was lethargic. He was running a fever, did not take antibiotics for post-op infection control and had previously received treatment for a plantar foot ulcer. Therefore, you should consider the mnemonic SEPTIC, which is as follows:16

   S: shock
   E: elevated temperature
   P: decreased platelets
   T: tachycardia/tachypnea
   I: increased white blood cell count
   C: confusion

   Sepsis is the presence of bacteria in the systemic circulation. Sepsis releases endotoxins and cause systemic illness. The dysfunctional neutrophils in a diabetic immune system prevent chemotaxis and phagocytosis of bacteria. Foot infections can quickly become systemic in part due to the anatomical connection of the pelvic veins draining into the spinal venous plexus, which has no anatomical valves. Research has also established that the epidural space, intervertebral disc, paraspinal soft tissues, lung, heart, kidney and bone all contribute to contiguous bacterial spread.

   If a foot ulcer becomes infested with bacteria and does not receive proper treatment, cellulitis can develop and quickly spread to deeper muscles, tendons and bone. This can lead to osteomyelitis. The hematogenous spread of bacterial pus from a localized foot infection to the systemic circulation is possible and can seed numerous toxins in any part of the body.17

   Sage, Pinzur and colleagues reported on three patients. The study demonstrated the effects of recalcitrant foot infections becoming global sepsis. Possible etiologies included psoas muscle abscess, cervical spine osteomyelitis, epidural abscess and septic shock.17

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