Algorithm for the Management of Diabetic Ketoacidosis
- American Diabetes Association From Diabetes Care Vol 29, Issue 12, 2006. Modifications from Diabetes Care, Vol 32, Issue 7, 2009.
- WikEM: Diabetic ketoacidosis
64M with a history of HFrEF (LVEF 20-25%), CAD, AICD (unknown indication), COPD, CKD III presenting with gradual onset shortness of breath, progressive bilateral lower extremity edema.
Examination consistent with severe acute decompensated heart failure presumed secondary to left ventricular dysfunction.
Telemetry monitoring with multiple episodes of nonsustained ventricular tachycardia.
In the ED, the patient developed worsening respiratory failure despite initiation of therapy, requiring endotracheal intubation. Continuous cardiac monitoring revealed persistent salvos of NSVT, progressing to slow ventricular tachycardia without device intervention.
Device interrogation revealed multiple events, 3 shocks, several ATP’s over the recorded period.
Non-specific IVCD, LAA, VPC
VT initiated by fusion complex
31F with autoimmune polyglandular syndrome (adrenal, thyroid and endocrine pancreatic insufficiency), presenting with fever and cough.
Evaluation consistent with sepsis presumed secondary to pulmonary source.
Telemetry monitoring initially with ventricular bigeminy, then nonsustained ventricular tachycardia.
In the ED, the patient developed pulseless ventricular tachycardia – apparently polymorphic. Chest compressions and epinephrine produced return of spontaneous circulation with recovery to baseline neurologic function.
ECG revealed prolonged QTc and chemistry panel notable for critical hypokalemia/hypomagnesemia.
Non-sustained ventricular tachycardia noted on telemetry monitoring
In some patients, NSVT is associated with an increased risk of sustained tachyarrhythmias and sudden cardiac death. In others it is of little prognostic significance.6,7,8
38M, unknown medical history, brought in after being found unresponsive next to an empty bottle of Seroquel. Presenting vital signs notable for blood pressure of 96/43, heart rate 103. Examination reveals tentatively protected airway (GCS E2 M5 V3, SpO2 100%, RR 14), normal pupil diameter and reactivity, dry mucous membranes with thick vomitus in oral cavity.
Laboratory evaluation was unremarkable, and there was no evidence of aspiration on chest radiography. ECG showed sinus tachycardia without QT prolongation. Blood pressure increased to normal range with fluid resuscitation. The patient’s mental status progressively improved and he was discharged after six hours of uneventful continuous cardiac monitoring.
|Class||Vital Signs||Mental Status||Pupils||Skin||Other||Examples|
|Other||HR > 100||1|
30 year-old female with a history of autoimmune polyglandular syndrome (adrenal, thyroid and endocrine pancreatic insufficiency), polysubstance use, brought to the emergency department by ambulance with reported chief complaint of fever. On presentation, the patient reported fever for one day, associated with cough. She was lethargic and confused, answering yes/no questions but unable to provide detailed history. She states that she has been taking her home medications as prescribed, which include hydrocortisone, fludrocortisone, synthroid and insulin. No collateral information was immediately available.
Additional history was obtained from chart review upon discharge. The patient was hospitalized two weeks prior with pneumonia and discharged after two days. For 2-3 days prior to presentation, she reported the following symptoms to family members: nausea/vomiting, cough, decreased oral intake, fevers, and palpitations – she did not take her home medications during this time.
|Gen:||Alert, fatigued, slow responses.|
|HEENT:||No meningeal irritation, dry mucous membranes.|
|Pulmonary:||Tachypnea, inspiratory wheezing and faint crackles at left and right inferior lung fields, appreciated anteriorly as well.|
|Neuro:||Alert, oriented to self, situation, not month/year. PERRL, EOMI, facial muscles symmetric, tongue protrudes midline without fasciculation. Peripheral sensation grossly intact to light touch and moves all extremities on command.|
The patient’s evaluation in the emergency department was concerning for severe sepsis secondary to suspected pulmonary source (given association of fever with cough, hypoxia and abnormal chest imaging findings). The patient had persistent alteration in mental status concerning for CNS infection. While preparing for lumbar puncture, cardiac monitoring revealed sustained polymorphic ventricular tachycardia without appreciable pulse. CPR was initiated, amiodarone 150mg IV push administered and at first pulse check a perfusing sinus rhythm was noted with immediate recovery of prior baseline mental status. Amiodarone load was continued and additional potassium sulfate (PO and IV) was administered. Review of telemetry monitoring revealed preceding 30-45 minutes of non-sustained ventricular tachycardia. The patient had two more episodes of sustained ventricular tachycardia requiring defibrillation. The patient was admitted to the medical intensive care unit for continued management.
#Sustained Ventricular Tachycardia
Initially attributed to critical hypokalemia and hypomagnesemia. However, after appropriate repletion serial ECG’s continued to demonstrate prolonged QT interval (possibly acquired secondary to medications, later review revealed multiple promotility agents for treatment of gastroparesis which could contribute to QT-prolongation including erythromycin and metoclopramide, also associated with endocrinopathies). Early echocardiography demonstrated global hypokinesis with estimated EF 30-35%. This was initially attributed to severe sepsis, as well as recurrent defibrillation. However, cardiac CT after resolution of acute illness showed persistent depressed ejection fraction, no evidence of coronary atherosclerosis. The presence of non-ischemic cardiomyopathy (may be attributable to chronic endocrine dysfunction or prior history of methamphetamine abuse) associated with malignant dysrhythmias warranted ICD placement for secondary prevention which the patient was scheduled to receive.
Attributed to pulmonary source given CT findings, healthcare associated and covered broadly. Mental status gradually improved and returned to baseline. CT head was negative, lumbar puncture deferred.
Unclear etiology. Adrenal insufficiency commonly associated with hyperkalemia and no history of surreptitious fludrocortisone use. Possibly secondary to GI losses. Improved with repletion.
#Autoimmune Polyglandular Syndrome
Started on stress-dose steroids in emergency department. Transiently developed DKA which was reversed appropriately and hydrocortisone was tapered to home regimen. Home levothyroxine was resumed.
|Constitutional||Weight loss, heat intolerance, perspiration|
|Cardiopulmonary||Palpitations, chest pain, dyspnea|
|Neuropsychiatric||Tremor, anxiety, double vision, muscle weakness|
|Neck||Fullness, dysphagia, dysphonia|
|Reproductive||Irregular menses, decreased libido, gynecomastia|
|Vital signs||Tachycardia, widened pulse pressure, fever|
|Cardiovascular||Hyperdynamic precordium, CHF, atrial fibrillation, systolic flow murmur|
|Ophthalmologic||Widened palpebral fissure, periorbital edema, proptosis, diplopia, restricted superior gaze|
|Neurologic||Tremor, hyperreflexia, proximal muscle weakness|
|Dermatologic||Palmar erythema, hyperpigmented plaques or non-pitting edema of tibia|
|Neck||Enlarged or nodular thyroid|
Essentially an exaggeration of thyrotoxicosis featuring marked hyperthermia (104-106°F), tachycardia (HR > 140bpm), and altered mental status (agitation, delirium, coma).
|Moderate (rales, atrial fibrillation)||10|
|Nausea/vomiting, abdominal pain||10|
|Constitutional||Weight gain, cold intolerance, fatigue|
|Cardiopulmonary||Dyspnea, decreased exercise capacity|
|Neuropsychiatric||Impaired concentration and attention|
|Reproductive||Irregular menses, erectile dysfunction, decreased libido|
|Integumentary||Coarse hair, dry skin, alopecia, thin nails|
|Vital signs||Bradycardia, hypothermia|
|Cardiovascular||Prolonged QT, increased ventricular arrhythmia, accelerated CAD, diastolic heart failure, peripheral edema|
|Neurologic||Lethargy, slowed speech, agitation, seizures, ataxia/dysmetria, mononeuropathy, delayed relaxation of reflexes|
|Musculoskeletal||Proximal myopathy, pseudohypertrophy, polyarthralgia|
Either primary due to adrenal gland failure (often secondary to autoimmune destruction), or secondary most often due to exogenous glucocorticoid administration (usually requiring more than 30mg/day for > 3wks).
|Gastrointestinal||Anorexia, nausea, cramping|
|Reproductive||Amenorrhea, decreased libido|
|General||Hyponatremia, orthostatic hypotension, low-grade fever|
|Primary||Hyperpigmentation, hyperkalemia, hyperchloremia, acidosis|
Unfortunately, this patient’s comprehensive clinical picture does not fit neatly into a particular category of endocrinologic pathology. Her underlying autoimmune disorder manifests both primary adrenal and thyroid dysfunction. Components of the patient’s presentation are suggestive of critical hypothyroidism (myxedema coma) including alteration in mental status, QT-prolongation and hyponatremia as well as possible precipitant of pneumonia. However, despite elevated TSH, the patient’s free T4 level was within normal range. Also absent was hypoventilation (the patient was appropriately tachypneic for degree of hypoxia and with resultant respiratory alkalosis) or bradycardia/hypothermia.
Similarly, adrenal insufficiency is typically associated with hyperkalemia, whereas our patient had critical hypokalemia that was determined to be at least a contributory factor to her ventricular dysrhythmia. The etiology of the patient’s hypokalemia remained unexplained.
|Anaphylaxis||Exposure to allergen||Abrupt onset, facial swelling||Stridor, wheezing, hives|
|PE||Immobilization, malignancy, prior DVT/PE, surgery, OCP||Abrupt onset, pleuritic chest pain||Tachycardia, hypoxia||ECG (RV strain)
CT PA, D-dimer
LE US (DVT)
|Pneumonia||Exposure, tobacco use||Fever, productive cough||Focal rales||CXR
|Pneumothorax||Trauma, thin male||Abrupt onset, chest pain||Decreased BS, subQ emphysema, JVD and tracheal deviation if tension||CXR
|Fluid overload||Dietary indiscretion, medication non-adherence||Orthopnea, PND||JVD, S3/S4, peripheral edema||CXR
|COPD/Asthma||Tobacco use, personal/family history||Progressive||Retractions, accessory muscle use, wheezing||CXR
US (distinguish from fluid overload)
|Malignancy||Tobacco use, weight loss||Hemoptysis||CXR
58 year-old female with no known past medical history, brought to emergency department by husband due to fatigue and weakness. The patient does not speak and cannot provide history. Her husband describes a progressive decline from normal baseline two weeks ago, noting lethargy/fatigue. Noted decreased speech and attention one week ago, and absent speech and requiring assistance with ambulation for the past two days. Thorough review of systems unremarkable excepting vomiting with decreased oral intake (tolerating fluids) and prior headache which resolved.
On examination, vital signs were normal, the patient was lying in bed and in no acute distress. The patient was non-verbal and did not follow commands (GCS E4-M5-V2). She was unable to comply with a thorough neurological examination, however pupils were equal and reactive, eyes tracked without nystagmus, no facial asymmetry noted, reflexes 1+ and symmetric in UE/LE, cannot participate in strength/sensory testing. Abdominal examination notable for infraumbilical and left-sided mass which elicits groans with palpation, though no rigidity or guarding. Mucous membranes moist, no skin tenting.
The patient was admitted to the medical intensive care unit. The following problem list details findings from the extensive inpatient evaluation.
#Altered Mental Status: The patient’s dramatically depressed level of consciousness improved gradually with correction of hyponatremia and the patient was alert, oriented and at baseline at the time of discharge. Evaluation included MRI brain which showed only chronic microvascular changes. A lumbar puncture was notable for isolated elevation of CSF protein. The patient was treated empirically for HSV encephalitis until CSF HSV PCR resulted negative. Neurology was consulted and identified increased CSF oligoclonal bands of unclear significance.
#Hyponatremia: Nephrology consulted, presumed SIADH based on urine studies (secondary to infection or malignancy). Corrected upon discharge.
#Pelvic Mass: Initially thought to arise from small bowel on CT abdomen/pelvis, after bladder decompression and transvaginal ultrasound, thought to arise from adnexa. Gynecology consulted, cyst characteristics (homogenous, fluid-filled) suggest benign process and tumor markers within normal limits. No acute intervention, drainage or biopsy warranted.
#Bladder distension: Unclear etiology, associated with mild/moderate hydronephrosis. Thought to be secondary to bladder outlet obstruction secondary to pelvic mass. Indwelling catheter placed, discontinued prior to discharge with successful spontaneous voiding trial and normal post-void residual.
|Exacerbation with head movement||+||–|
|BPPV||Otolith||Brief, positional episodes||Nausea, vomiting, absent auditory symptoms.||Dix-Hallpike positive|
|Vestibular neuronitis||Viral, post-viral inflammation of vestibular portion of CNVIII||Acute and severe, subsiding over days.||Nausea, vomiting, absent auditory symptoms.||Head thrust abnormal|
|Meniere||Endolymphatic hydrops||Recurrent, lasting hours||Tinnitus, hearing loss.||SNHL|
|Vertebrobasilar insufficiency||Atherosclerosis (vascular risk factors)||Acute onset, recurrent episodes if TIA||Headache, gait impairment, diplopia, absent auditory symptoms.||Neurologic deficits|
|Cerebellar stroke||Atherosclerosis (vascular risk factors)||Acute and severe||Headache, dysphagia, gait impairment||Dysmetria, dysdiadochokinesia, ataxia, CN palsy|
|Brainstem stroke||Atherosclerosis (vascular risk factors), dissection||Acute and severe||Dysphagia, dysphonia, gait impairment, sensory disturbances||Loss of pain/temperature on ipsilateral face, contralateral body, palatal/pharyngeal paralysis|
|MS||Demyelination||Subacute onset||History of other, variable symptoms||INO|
Normal head impulse, direction-changing nystagmus, or skew deviation suggests stroke.
|Migraine||Unilateral||Hours to days||Throbbing||Photophobia, phonophobia||Atypical migraines with neurological findings (basilar, ophthalmoplegic, ophthalmic, hemiplegic)|
|Tension||Bilateral||Minutes to days||Constricting||None|
|Cluster||Unilateral, periorbital||Minutes to hours||Throbbing||Conjunctival injection, lacrimation, rhinorrhea, miosis, eyelid edema||Males 90%, triggered by EtOH.|
|Opening pressure||>15cm H20||Normal||Normal|
|Medication||Dose (adult)||Dose (peds)||Comment|
|Lorazepam||4mg IV||<13kg: 0.1mg/kg (max 2mg)
|Repeat in 10min|
|Midazolam||10mg IM||0.2mg/kg IM (max 5mg)||Repeat in 10min|
|Midazolam||10mg buccal||0.5mg/kg buccal (max 5mg)||Repeat in 10min|
|Fosphenytoin||20mg PE/kg IV|
|Phenytoin||20mg/kg IV||May cause hypotension|
|Propofol||1-2mg/kg bolus then 20-200mcg/kg/min|
|Pentobarbital||5-15mg/kg bolus then 0.5-5mg/kg/hr|
|MgSO4||6g IV over 15min||Eclampsia (20wks gestation to 6wks post-partum)|
|Pyridoxine||0.5g/min until seizures stop, max 5g||INH ingestion|
|3% saline||100-200mL over 1-2h||Confirmed hyponatremia|