Management Of Diabetic Emergencies Flashcards
What are the 3 acute diabetic emergencies
1) DKA
2) HHS (hyperglycemia, hyperosmolar mild ketosis syndrome)
3) hypoglycemia
What is the diagnostic A1c level for diabetes
> 6.5%
Pathophysiology behind DKA
1) Excess glucose causes osmotic diuresis which results in loss of water, potassium and magnesium
- also some mild sodium
2) Excess hypokalmeia produced by excess glucose results in inhibition of insulin releases which results in a vicious snowball effect
3) This eventually leads to dehydration/starvation in cells which leads to:
- cells decreasing AA uptake and accelerates proteolysis
- adipose tissue not clearing circulating lipids which causes excess metabolism into (B-hydroxybuterate and acetoacetate) ketoacids which builds up in blood
- increased ketosis and starvation causes decreased ketone use and more stays in plasma
- uninhibited glycogen and catecholamine releases which further promotes gluconeogenesis and glycogenolysis
4) All of this promotes excessive ketone production from excess FFAs but ALSO decreases total ketone use.
- this results in an even more hyper osmotic state in the blood and excess ketones that just sit around produce acidosis effect
5) All of this hyperosmolarity results in increased acidosis and increased glucose release in the blood
Causes of DKA
Most common = lack of insulin use
Can also be aggregated in diabetic patients by MIs, infections.
this is most common in DM1 but can be seen in DN2
Symptoms of DKA
On top of having the three P’s
- abdominal pain and cramping (in adult diabetics = look for secondary cause in the GI; in children = usually idiopathic and signals DKA as primary cause)
- tachycardia, tachypnea
- AMS
- hypotension
- acetone breath
- significant voiding of bladder
- dry mucous membranes an dehydration symptoms
note DKA almost never produces pyrexia by itself, so if a fever is present = must search underlying infection
Lab values in DKA
80% chance the glucose is >350
- however 20% show normal glucose so this isn’t diagnostic
Hyponatremia/kalemia /magnesia
- note that initially will show hyperkalemia since potassium will leave intracellular to make up for low potassium in blood
Low bicarbonate and low pH
- *ketones in urine and blood elevated as well as elevated blood osmolarity**
- most sensitive
Often shows elevated anion gap metabolic acidosis
- however if the patient is excessively vomiting = may be normal gap
Elevated WBC
Why is ECG important in DKA
The levels of potassium can be measured with this initially as well as be prepared for arrthymias
Initially = hyperkalemia
- peaked T waves with short QT intervals and widened QRS
Later = hypokalemia
- flattening of T waves and inversion of T waves
- also shows visual U wave (really bad)
- eventually leads to Torsades (replace magnesium before potassium otherwise nothing happens)
When do you incubate a patient
GCS is less than 8
Significant AMS is present or coma
No protection fo airway or not able not able to ventilate properly
if patient is in DKA and needs intubation = must continue to hyper ventilate to prevent worsening of acidosis
What should you do in patients who have shock with DKA
Hydrate aggressively and look for causes of shock that is NOT DKA to rule out extrinsic causes
- sepsis
- cardiogenic
- hypovolemic
**usually give greater than 2L per 2hr
Caveats to treatment of DKA
On top of hydrating and intubating as needed:
- must give insulin via a drip with hydration
- DONT hydrate or give insulin too fast (risk increased cerebral edema and worsens acidosis) Usually give 2L 0.45% NS in first two hours and give insulin drip of 0.1g/kg
- NEVER GIVE insulin if potassium is lower than 3.3 mEq/L (must correct this first)**
Once glucose is under 300 mg/dL = give dextrose with normal saline (still 0.45%)
To correct electrolytes
- magnesium = usually give 1-2 g MgSO4- ( increase dose if torsades is present)
- phosphorus = nothing
- sodium = nothing other than NS
- potassium = add 20-40 mEq KCL to each liter of saline if potassium is <5.5. If under 3.3 = give more than 40 mEq/L
- *USUALLY DONT GIVE BICARBONATE**
- makes acidosis worse and worsens electrolyte abnormalties
- only time to give = cardiac arrhythmia present of alcoholic induced DKA
Hyperglycemic hyperosmolar state (HHS)
More common in T2DM but can be in Type 1 also
Characterized By
- mild ketosis or no ketosis
- metabolic acidosis with anion gap
- prominent CNS changes (seizures are more common)
- marked hyperglycemia
- severe dehydration
- can look similar to DKA however*
- is more common in elderly
- longer prodromal than DKA (takes longer than a day)
- 15% may also show GI bleeding, pneumonia, cardiac issues, vascular issues
commonly associated with renal insufficiency, gram (-) sepsis or pneumonia, GI bleeding
Lab values in HHS
Glucose is usually >700
-they are far more dehydrated
Hypotensive
Mild fever
Electrolytes are more wider abnormality than DKA
- also sodium is usually less severely declined
- DONT use potassium equation to overcorrect in this patient since pH is normal
- *pH is usually normal and there are no serum ketones
- also bicarbonate level is >15 usually
**BUN is usually higher than in DKA (>50 compared to 25-50 respectively)
WBC is usually normal unless underlying infection
Management of HHS
Very similar to DKA
Start with insulin at 0.1/kg and 1-2 L 0.45% NS every 1-3 hrs until glucose is <300, then switch to Dextrose in 0.45% NS every 1-3 hrs
Same electrolyte correction measurements
must search for the cause of this and it’s usually lack of insulin but have to rule out infections or acute stress events
*NOTE: cerebral edema is more common in HHS than DKA since glucose is usually even high in HHS
What is the most dangerous complication of diabetes
Hypoglycemia
- is more common in T1DM and is the most common cause of coma in T1DM
- severe hypoglycemia = <50 mg/dL glucose
Caused by excess insulin = most common cause
- also overuse of oral hypoglycemic agents (especially sulfonylureas since it stays in the body forever due to long half life) is the most risky drug in T2DM treatment for this**
- increased energy and output/exercise can be a cause also
- alcohol dependence and malnutrition can make it easier to hit hypoglycemia (give thiamine first for alcoholics)
What is the somogyi effect?
Iatrogenic hypoglycemia inT1DM
- caused by excess insulin dosing which causes hypoglycemia while the patient is sleeping
- *This leads to rebound hyperglycemia when the patient awakens (growth hormone, cortisol and glucagon are released in high quantities in the morning in general, but in a night time hypoglycemic event = release even more)**
- this can lead to misrepresentation of poor control resulting in increased insulin prescription from the doctor and further making this worse and lead to chronic hypoglycemic**
Clinical features of hypoglycemia
Usually present once blood sugar is <40-50 mg/dL
CNS issues predominant
- strange behaviors
- seizures
- Coma
Also excess epinephrine due to hypoglycemia
- sweating
- tremors
- tachycardia
- hunger
- nervousness or “impeding doom”
How to test for hypoglycemia causes
1 = blood glucose test before treating bit isnt always possible
Look for other causes
- alcohol excessive use (check ABG and BMP)
- factitious hypoglycemia (overuse of endogenous prescribed insulin or use of herbal medications that block insulin degradation) = check C-peptide levels
- if factious = high insulin but low-normal levels of peptide C
How to treat hypoglycemia
Mild symptoms = give oral glucose and monitor (usually able to discharge)
Severe symptoms = give D50W IV glucose
- also MUST give seizure prophylaxis
- can also give glucagon orally or IM if you cant get an IV
Alcohol abuse or malnutrition = GIVE THIAMINE 1st before glucose administration
In children <8 years that need IV glucose = give D25W instead of D50W
- if a patient is ODing on oral hypoglycemic agents (treatment for DMtype 2 and especially sulfonylureas) = must give glucose with octerotide (prevents refractory hypoglycemia due to insulin release)**
- YOU ALSO MUST ADMIT THESE PATIENTS ALWAYS
What is the most importaint determinant of mental status in a patient with DKA?
The osmolarity in the patient
- hyperosmolar = severe AMS
- hypoosmolar = severe AMS
Sodium and potassium equation in DKA
In DKA and excess glucose, can result in pseudohyponatremia and pseudohyperkalemia
Sodium equation = add 1.6 mEq/L for every 100 mg/dL above normal glucose levels
Potassium equation = subtract 0.6 mEq/L for every 0.1 below normal pH
Normal glucose = 100 mg
Normal pH = 7.4
What is associated with cerebral edema after DKA?
Bicarbonate therapy (DONT GIVE unless MI is present)
Blood glucose is less than 250 mg (DONT use excessive insulin)
Elevated BUN
Hypocariba (low bicarbonate)
What are the criteria to send a DKA patient home
Have a excellent outpatient follow-up
They need to understand how to properly administer IM. IV does of bolus insulin and be well hydrated
Also needs only mild acidosis or no acidosis at discharge
What must be fixed first before giving insulin for hyperglycemia?
The potassium levels
- insulin drips can cause hypokalemia
- must make sure potassium is at least 5.0
How to give insulin?
IV insulin 0.1 U/kg/h up to 10 hrs per hour on continuous drip
DONT give bolus
**if blood sugar gets too low (<250) = give Dextrose 5% in 0.45% NS
Cerebral edema in DKA/HHS
Occurs after 6-10 hrs after treatment and is far more common in children
- begins as AMS and severe headache
- mortality is 90% so you need to teach and ideally just prevent this
High yield factors that suggest HHS over DKA
Glucose >600 mg/dL
Serum osmolarity > 320 mOSM/L
May show normal pH or acidotic
- however, NO KETONES/KETOSIS
Pseudohyponatremia
Classically seen in elderly
Classically seen in type 2 diabetics
Insulin is usually present
High yield DKA factors
Hyperglycemia but usually not greater than 600
Anion gap metabolic acidosis due to excess ketones is always present
- most common ketone is B-hydroxybutyrate**
Often presents with ketosis breath and kussmaul breathing
No insulin present
Usually in diabetes type 1 patients
What is the most common associated Disease in HHS patients?
Chronic kidney injuries
Thyrotoxicosis/thyroid storm
Is usually caused by an acute stressor in a patient with undiagnosed or uncontrolled Graves’ disease/hyperthyroidism
- stressors = sepsis, surgery, MIs, CVAs, physical trauma, ingestion of levothyroxine
Mild Symptoms
- tachycardia
- palpitations
- tremor
- weight loss (usually extreme)
- nervousness
Moderate symptoms
- new onset atrial fibrillation
- mild CHF
- diarrhea
- nausea/vomiting
Severe/thyroid storm only symptoms:
- fever
- AMS (agitation, psychosis
- severe CHF
- jaundice
- HR > 130 at rest
most common cause of death = cardiovascular collapse
Labs:
- TSH/T3/4 values
- anti-TBO antibodies
- CMP (check for jaundice and electrolytes and glucose)
- cardiac panel, troponin (check for heart damage)
- CBC = elevated WBC
- ABG = respiratory acidosis or alkalosis can happen
- ECG
- BP/RR/HR = all very elevated
Treatment;
1) Start on BBs (propranolol) = 60-80 g PO every 4 hrs (can use IV propranolol o.5-1.0 IV slow push and then repeated 1-2 mg every 15 minutes)
2) give PTU 500-1000 mg loading dose and then 250 mg every 4 hrs (slow down T3/T4 levels)
3) ** AFTER 1hr of giving PTU = give potassium iodide (SSKI) 50 mg drops PO every 6 hrs
4) also can give hydrocortisone 300 mg IV bolus and then 100 mg three times a day for several days
What are the most common cardiac complications of thyroid storm?
1) Atrial fibrillation with rapid ventricular response
2) High output HF
- T3 increases inotropic and chronotropic effects
- this is the most common cause of death
Myxedema coma
Usually caused by underlying hypothyroidism that is severely precipated via acute stressor
- common = infections, MI, post surgery, extreme cold exposure, sedative drugs including opioid use
History:
- no craving of salt or weight loss
- gradual fatigue and edema complaints
- no history of diuretics or lithium
- should show no CNS symptoms
- may show goiter
Symptoms:
- decreased AMS
- hypothermia
- hypotension, bradycardia
- hyponatremia, hypoglycemia (both usually severe)
- respiratory acidosis due to hypoventilation
- may show swollen tongue and puffiness of the face
- WILL go to coma if not treated
Labs:
- get thyroid levels (low T4 and TSH high or normal)
- also may see normal or high ACTH if severe hypothyroidism with high cortisol**
- low serum osmolality and high urine osmolality
- blood and urine cultures ( try to find infection
- EKG and MRI (EKG = T wave inversions and bradycardia)
- ABG = respiratory acidosis with or without compensation
Treatment:
1) thyroxine 600 ug IV
2) give hydrocortisone 200 mg IV
3) start on 0.9% NS infusion 100mL/hr to correct hyponatremia (DONT OVERCORRECT TO QUICKLY)
4) can give passive warming via heating blankets
5) can give cefuroxime to treat any underlying infections
