Endo + Electrolyte Emerg.

Presentation:
- mild: may be asx
- BG >180 (renal threshold) = polyuria/dipsia/phagia/wt loss
- MOD: abd pain, Kussmaul resp, hypoTN, ketotonic breath, tachycardia
- SEV: seizures, focal weakness, lethargy, coma, death

complication: cerebral edema- usually in children and young adults; preceded by HA, lethargy, neuro, bradycardia, respiratory arrest

DDX:

HHS- hyperosmolar hyperglycemic state

Hyperglycemia, hyperosmolar, dehydration, *WITHOUT significant ketoacidosis*

usu. in T2DM; older people

MCC: poorly controlled T2DM w/underlying infxn

DKA

absolute insulin deficiency; hyperglycemia, anion gap acidosis; dehydration

usu. in T1DM; younger people

MCC: infection, disruption of insulin therapy, presentation of new onset DM

Tx:
- Mild-mod: may only need IV fluids
- DKA and HHS:
1. correct intravascular vol. depletion: NS 1L/hr; LR may be better option to avoid hyperchloremic non-anion gap metabolic acidosis
2. manage electrolyte abnormalities: replace K+ and Bicarb
- K+ b/w 4-5 is NL
>5.5= insulin infusion
3.5-5.5= add K to fluids
<3.5= hold insulin, add K and restart insulin later
3. insulin replacement: IV infusion of regular insulin (preferred); at 10units/hr in 70kg pt
4. ID underlying cause and tx that - infx= abx

Pres:

Altered Autonomic: palpitations, tremor, anxiety, tachycardia, HTN, increased hunger, diaphoresis, paresthesias

Diminished cognitive: HA, dizzy, visual disturbances, focal neuro deficit, altered consciousness, seizure, coma, low GCS

Etiol:

common w/DM pts that intentionally/unintentionally take too much insulin
- meds: insulin, insulin secretagogues (sulfonylureas, meglitinides)

critical illness

ethanol consumption, liver disease

fasting state

insulin secreting tumor

Diagnostics:
- point of care glucose testing
- additional testing to determine causes, or conditions that may mimic hypoglycemia

Tx:

DEXTROSE
- Oral: preferred if awake/alert- 30g of carb
- IV: if unable to give PO

Glucagon: if NO IV access and PO cannot be safely given
- Adults: 1mg IM
- PEDS <20kg: .5mg IM

Octreotide: in persistent hypoglycemia not responsive to other therapies (ie. sulfonylurea toxicity) - chk glucose q1-2h after starting octreotide

Pres: can be underwhelming!
- weakness and/or paresthesias
- SEVERE? = cardiac (significant), neuromuscular- muscle cramps, generalized weakness; GI: N/V/D
PE: extrasystoles; pauses/bradycardia; decreased DTR; decreased strength on neuro; look for fluid overload and dialysis access sites

Cardiac pres: 2nd or 3rd degree heart block; wide complex tachycardia; progression to vFib; asystole

Etiol:

Decreased renal clearance- CKD, AKI

increased release from intracellular space- hemolysis, rhabdo, burns, crush injury

altered transfer to intracellular space- acidosis, insulin deficiency, succinylcholine

EKG: marker for clinically significant hyperkalemia
1. tall, peaked T waves (>6.5)
2. flattening of p wave, prolongation PR interval and widening of QRS (>7)
3. loss of p waves leading to sine-waves: fusion of wide QRS w/ST-T segments (8-10)

Tx: if ECG manifestations or pt is hemodynamically unstable then first tx is STABILIZE MYOCARDIUM
1. Stabilize myocardium w/Calcium gluconate or Ca chloride - this will reverse ECG changes
2. intracellular K transfer w/regular insulin
3. decrease total K w/Furosemide
- can also use Kayexelate (binds K, not used much), Hemodialysis (if hemodynamically unstable, or if pt is dialysis dependent), or Patiromer (binds K)

s/sx: Catecholamine EXCESS= HTN crisis- HA, CP, palp, SOB, sweating

Dx: Fhx, elevated urinary catecholamine; CT or MRI of abd/pelvis; MIBG scan to detect tumors not seen on CT or MRI

Tx: Control HTN w/alpha blocker; BB AFTER alpha blockage
*avoid BB alone

RF: pregnancy, head trauma, pituitary radiation, dopamine agonist tx

CT (non contrast) and MRI may show sellar mass and hemorrhage

Tx: admit ICU + CS + neurosurg consult + endo, ophthalmology, and neurology

s/sx: severe hypothermia, hypoventilation, hyponatremia, hypoglycemia, hytoTN, rhabdo, AKI

Tx: Thyroxine IV bolus