CC
A 53-year-old male with a history of type 1 diabetes mellitus (DM1) presents to the emergency department (ED) complaining of swelling of mouth and neck, making it difficult for him to swallow.
HPI
The patient states he started having pain in his lower right jaw 1 month ago when he had a tooth pulled, despite taking clindamycin. (Empiric clindamycin is not recommended because of resistance of oral streptococci, such as Streptococcus anginosus [milleri] group [20%–30%], and anaerobes, such as Prevotella spp. and Porphyromonas spp. [31%–38%].) He presented to the same hospital 2 weeks ago with right jaw pain and swelling and was diagnosed as having a right dental abscess. The dentist on call saw the patient and performed an incision and drainage bedside under local anesthesia and placed a drain for continued source control, which was removed a couple days later as an outpatient.
The patient states he was given a prescription for amoxicillin and has been compliant with oral hygiene and chlorhexidine mouthwash. (Penicillin alone cannot fight the β-lactamase–producing oral anaerobes, and penicillin monotherapy is no longer recommended.) However, since the drain was removed, he has had increasing pain and swelling. (Source control through drainage is the most important therapeutic modality for pyogenic odontogenic infections, and premature removal of the drain is not advised.) Swelling has since progressed to the point that it is hard for him to open his mouth and swallow, causing significant discomfort and poor oral intake.
Swelling has rapidly progressed during the past 24 hours, which is why he presented to the outside facility yesterday for evaluation. The workup was also notable for hyperglycemia (blood glucose > 1000 mg/dL), acute kidney injury (AKI) (creatinine, 1.99 mg/dL) and hyperkalemia (potassium, 7.5 mmol/L) (some of the key presentations of the hyperglycemic emergencies, namely diabetic ketoacidosis [DKA] in DM1, and hyperosmolar hyperglycemic state [HHS] in type 2 diabetes [DM2]). The patient received intravenous (IV) normal saline (to replete volume and reverse AKI), 20 units of regular insulin (to treat hyperkalemia), and IV Unasyn (ampicillin–sulbactam) (the preferred antibiotic regimen in odontogenic infection in absence of penicillin allergy). Given the extent of the infection, the patient was transferred to our hospital to be managed by the oral and maxillofacial surgery service.
PMHX/PDHX/medications/allergies/SH/FH
The patient was diagnosed with DM1 (an autoimmune destruction of pancreatic beta cells) in his 20s and has been taking insulin since. (The two main types of diabetes are type 1 [DM1] and type 2 [DM2]. DM1 used to be called juvenile-onset [usually develops in children or young adults but can occur at any age] or insulin-dependent diabetes. [There is no insulin production in DM1, hence the need for daily insulin injections or an insulin pump.] DM2, on the other hand, used to be called adult-onset or non–insulin-dependent diabetes. In DM2, despite adequate production of insulin initially, the cells do not respond to insulin the way they should. The insulin receptor is a tetramer of two ligand-binding alpha and two transmembrane beta subunits joined by disulfide bonds. These subunits are coded by a single gene, and mutation in either the structural gene or some of the processing steps may lead to insulin resistance. The insulin may bind the receptor normally, but the signaling cascade may not be triggered. β-cell compensation results in hypersecretion of insulin, ultimately leading to β-cell burn-out. DM2 is more likely to occur after 40 years of age, in overweight patients, and in those with a family history of diabetes. Unfortunately, because of sedentary lifestyles and the fast-food epidemic, DM2 has become more prevalent in younger people, including adolescents.) Our patient takes glargine (Lantus, a long-acting synthetic insulin that provides a steady concentration of insulin) once a day and preprandial lispro (Humalog, a rapidly acting insulin) three times a day. He is currently being followed by his family practitioner. His medical history also includes hypothyroidism (patients with DM1 are more likely to have a co-occurring autoimmune disorder; 30% of the population with DM1 also have autoimmune hypothyroidism, and 10% of them have concurrent celiac disease), Parkinson’s disease, stage 3 chronic kidney disease (a common sequela of DM), hypertension, hyperlipidemia, and nephrotic syndrome. His other medications include amlodipine, losartan, aspirin 81 mg, atorvastatin, bisoprolol, carbidopa–levodopa, levothyroxine, and ergocalciferol. He has had no prior surgeries but was hospitalized for hypoglycemia twice during the previous year. (Previous episodes of hypoglycemia are a risk factor for future episodes.) He reports that his blood glucose was between 80 and 160 mg/dL during the past year, as measured with his home Accu-Chek device. (The ideal preprandial blood glucose level is 90–130 mg/dL.) However, he lost his device and stopped monitoring his blood glucose a couple of months ago. He also has missed several of his primary care and diabetes check appointments. (Poorly controlled blood glucose decreases the ability to fight infections.)
There is no family history of diabetes mellitus. (DM1 has a strong association with HLA-DR3, DR4, and DQ alleles; however, a family history is often lacking. A positive family history is often seen with DM2.)
Examination
General. The patient is a thin, visibly uncomfortable male (unlike patients with DM2, those with DM1 are frequently thin or cachexic). His speech is muffled, but there is no breathing difficulty or drooling.
Vital signs. His vital signs are stable, and he is afebrile. His oxygen saturation is 97% on room air.
Maxillofacial. The patient has right lower and midfacial edema and induration, submental edema and induration, and left submandibular induration. There is tenderness to palpation in all these areas. He presents with restricted mouth opening to 1.5 cm.
Intraoral. Examination is limited because of trismus and pain, but from the limited examination, there appears to be purulence draining intraorally from the posterior right mandible. Oral hygiene is poor with multiple carious teeth. The floor of the mouth is indurated and slightly elevated.
Labs
In the ED, his labs were notable for hyperkalemia to 6.1 mmol/L (lack of insulin means potassium cannot enter the cells and is maintained in the extracellular space), bicarbonate of 28 mmol/L (normal serum level is 22–29 mmol/L, the primary buffering mechanism for acidosis), anion gap of 14 mmol/L (>10 in mild DKA, >12 in severe DKA, and usually within normal limits [8–12 mmol/L] in HHS), creatinine 2.41 mg/dL (AKI secondary to hypovolemia), blood glucose of 728 mg/dL (HHS usually presents with much higher blood glucose values than DKA), white blood cell (WBC) count of 21.1 × 10 9 /L (indicating severe infection), and a platelet count of 100 × 10 9 /L (thrombocytopenia). ECG did not reveal any changes associated with hyperkalemia. (The expected ECG changes in hyperkalemia include peaked T waves, P wave flattening, PR prolongation, and widened QRS complex.) Urinalysis showed a ketone level of 15 mmol/L (normally no ketones are found in urine), 30 to 49 red blood cells (RBCs) per high-power field (hpf) (a normal result is ≤4), greater than 300 mg of protein (normally, there is <150 mg of protein in the urine per day), and a WBC count of 4 WBC/hpf (normal, 0–5).
To better assess the patient’s glucose control, we ordered a glycosylated hemoglobin (HbA 1c ) level test. (HbA 1c is an effective, objective tool for assessing patient compliance and long-term hyperglycemic status. Prolonged elevation of serum blood glucose causes nonenzymatic, irreversible glycosylation of hemoglobin in RBCs. Because the life expectancy of RBCs is 120 days, the HbA 1c gives an estimate of glycemic control during the past 90 to 120 days. An HbA 1c greater than 6% is consistent with diabetes, and a value greater than 7% is indicative of poor glycemic control. Therefore, the HbA 1c directly correlates with poor glycemic control for the previous 3 to 4 months.) HbA 1c was 9.1 in our patient, indicating poor diabetic control.
Imaging
For the surgical management of patients with diabetes mellitus, the need for adjunctive imaging studies is dictated by the clinical findings and suspicion of sources of infection or pathology. Nonodontogenic sources of infection, including parotitis and lymphadenitis, should be considered in all patients. Our patient had a maxillofacial computed tomography (CT) scan done, which showed multi-space odontogenic abscesses involving the right parapharyngeal space but no airway deviation; right submasseteric, pterygomandibular, and infratemporal spaces (collectively called the masticator space); right sublingual and submandibular, submental, and left sublingual and submandibular spaces (collectively known as Ludwig’s angina).
Assessment
A 53 year-old male with multispace odontogenic abscesses, including Ludwig’s angina, complicated by poorly controlled diabetes, impending DKA, and potential airway compromise.
Hepatocytes, in the absence of insulin (DM1) and in response to the presence of glucagon, increase the process of gluconeogenesis and glycogenolysis to make more glucose. The absence of insulin also leads to increased lipolysis by hepatocytes. The free fatty acids are then converted into acetyl CoA through a process called beta-oxidation. In energy-deficient states, such as starvation, acetyl CoA is metabolized into ketone bodies through the process of ketogenesis. The final products of this process are aceto-acetate and β-hydroxybutyrate, which can serve as energy sources in the absence of insulin-mediated glucose delivery. Ketone bodies have a low pKa and cause metabolic acidosis.
Another major issue in a hyperglycemic state is hypovolemia. Glucose freely filters in the glomerulus and fully reasorbs in the proximal convoluted tubule. The overflow of glucose into the bloodstream overwhelms the resorption capacity of the proximal convoluted tubules, and the remainder of the filtered glucose is passed into the urine. Increased urine glucose causes osmotic diuresis and volume depletion. The renin–angiotensin–aldosterone system tries to compensate for the loss of water and volume. Aldosterone pulls sodium back into the bloodstream, and water follows. However, this is not enough to counteract the osmotic diuresis. Moreover, reabsorption of sodium comes at the price of potassium excretion into urine. As a result, the patient will be in a state of total potassium deficit despite their hyperkalemic plasma.
The presence of significant amounts of ketones in plasma and urine and marked metabolic acidosis are the distinguishing features of DKA. HHS, also known as hyperosmolar nonketotic state or HONK , is primarily seen in DM2 and presents with increased plasma osmolarity (>320 mOsm/kg; normal low is 280 mOsm/kg, and normal high is 300 mOsm/kg) caused by profound dehydration and hemoconcentration.
The American Diabetes Association categorizes the severity of DKA as follows:
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Mild: blood pH of 7.25 to 7.30 (normal, 7.35–7.45) and serum bicarbonate of 15 to 18 mmol/L (normal >20) in an alert patient
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Moderate: blood pH of 7.00 to 7.25 and serum bicarbonate of 10 to 15 mmol/L with potential mild drowsiness
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Severe: blood pH less than 7.00 and serum bicarbonate less than 10 mmol/L with possible stupor or coma
Our patient had an arterial blood pH of 7.4 and a normal bicarbonate level, which rules out metabolic acidosis. (The deficiency in insulin [either absolute deficiency or a relative deficiency caused by excess counterregulatory hormones] is more severe in DKA compared with HHS. The small level of residual insulin secretion in DM2 is sufficient to minimize the development of ketoacidosis but does not control hyperglycemia.) The elevated serum osmolality (348 mOsm/kg) indicates a diagnosis or component of HHS but may also be seen in DKA. Although acidosis and ketonemia may be present in HHS, they are not as pronounced as they are in DKA. It should be noted that DKA and HHS may have overlapping features because DKA may also present with hyperosmolarity. The acidosis in DKA causes distressing symptoms (e.g., nausea, dyspnea, abdominal pain), driving the patient to seek care earlier. In addition, patients with DKA are much younger on average and have higher glomerular filtration rate than those with HHS. As a result, patients with DKA excrete more glucose in urine, limiting the hyperglycemia. Although mostly seen in patients with DM2, the working diagnosis for our patient was HHS because of the initial blood glucose greater than 1000 mg/dL, the elevated serum osmolality, a normal bicarbonate level, and a normal to mildly elevated anion gap.
Treatment
The patient was admitted to the medical intensive care unit (MICU) for the management of his emergency (patients with DKA or HHS should be admitted to the ICU) and close monitoring of airway before urgently going to the operating room (OR) for incision and drainage of multiple space abscesses. The MICU recommended improving the electrolyte derangements (potassium was still 6.2) before planned surgery unless surgery was emergently necessary. The patient was monitored on telemetry in the meantime. This is a complex situation, and the risk vs. benefit of a delay in definite surgical care should be discussed among the surgeon, the anesthesiologist, and the intensivist on a case-based basis. An airway emergency or impending airway compromise cannot wait and should be taken care of promptly. The patient received 26 units of Lantus and 1 L of lactated Ringer solution while in the ED, and fluid boluses and insulin drip continued in the MICU. The patient’s potassium was corrected to 4.4, and his blood glucose decreased to 113 mg/dL in 4 hours and was emergently taken to the OR for incision and drainage. Box 108.1 summarizes the strategies in the management of DKA. Treatment of HHS is based on the same concept and algorithm with some modifications. For instance, it needs more free water and greater volume replacement (caution for heart failure in elderly with preexisting cardiac issues).
