Endocrine: DM Types 1 & 2, Hypoglycemia, DKA, & Diabetic Emergencies (HHS, DI, SIADH )

normal glucose fasting

70-99 mg/dL

glucose intolerance

100-125 mg/dL

what BG level indicates diabetes

> or equal to 126 mg/dL

insulin is the

• key

• it opens the door to let glucose into the cells

type 1 DM

• autoimmune disease

• no insulin is produced

• the pancreas destroys cells that produce it

• WE WILL GIVE INSULIN

type 1 DM continued

• muscle unable to use glucose due to low insulin

• increased glucose due to low insulin

type 2 DM

• not able to move glucose into the cell using the insulin they have

• obesity and other factors that lead to insulin resistance

DM symptomology

3 p’s (usually seen more with >200 BG, glucose pulls water with it and glucose spills into the urine)

• polyuria

• polydipsia (thirsty)

• polyphagia ( eat more since cells are starved)

• fatigue

• muscle cramps

• nausea

• headache

GLUCOSE CANT MOVE INTO THE CELLS

treatment for type 1 DM

• must HAVE INSULIN

  • combo of short and long acting

• diet, exercise, infection vigilance !!!!!

glucose is a

chemical irritant

—> causes vascular damage to the eyes, kidney, brain

type 2 DM treatment

• weight loss/control

• diet, exercise

• oral agents + insulin

  • Metformin (decreases how much glucose is is absorbed from food)

type “1.5” DM (mix of both symptoms)

• combo meds, diet, exercise, and weight control

• SICK DAYS

• foot care

• cardiac care

• kidneys

rapid acting insulins are

• Lispro (humalog)

• aspart (novolog)

• glulisine (apidara)

rapid acting insulins onset

15 minutes

rapid acting insulin peak

60-90 minutes

short acting insulin’s are

• regular (humilin, novolin)

short acting insulin onset

30 min-1hr

intermediate acting insulin are

NPH (humulin N, Novolin N)

intermediate acting insulin onset

2-4 hrs

long acting insulin are

• glargine (lantus)

• determir (levemir)

long acting insulin onset

1-2 hrs

patient education for DM

• Disease process

  • which type they have

• lifestyle changes

  • activity, diet, need for care

• Meds

  • importance

  • actions, dosing, how to

• foot care

• cardiac consideration

patient education continued

SICK DAYS

• Ideally, instructions from health care provider

• Often mistakenly think less insulin / meds needed

• Need closer monitoring

• Fingersticks more frequent

• Insulin

  • Use rapid / short acting, no long acting

  • Pump – ensure proper functioning

  • Oral agents

• If tolerant, per instructions from HCP

• Consider calling primary when become ill

• Continued nausea / emesis – seek medical care

pancreatic disorders in the critically ill patient

• Stress-induced hyperglycemia

• Diabetic ketoacidosis (DKA)

• Hyperosmolar hyperglycemic state (HHS)

• Hypoglycemia

stress induced hypoglycemia risk factors

• Diabetes (diagnosed or undiagnosed)

• Advancing age

• Administration of exogenous catecholamines (epi/noepi)

• Glucocorticoid therapy

• Enteral or parenteral nutrition therapy

• Medications

• Obesity

• Pancreatitis, cirrhosis

adverse effects of DM

• Immune suppression

• Cerebral ischemia/stroke

• Dehydration/osmotic diuresis

• Impaired wound healing

• Endothelial dysfunction/thrombosis (stroke, clot, DVT)

• Decreased erythropoiesis

• Impaired gastric motility

clinical managment

Establish euglycemia

• Target glucoses of 140 to 180 mg/dL

• Insulin protocol (SUBQ or Drip)

stress and critical illness

• Hyperglycemia

  • Excessive hepatic glucose production

  • Relative hypoinsulinemia

• Adrenal insufficiency

  • Primary and/or secondary dysfunction

• Thyroid dysfunction

hyperglycemia crises

• Reduction in circulating insulin with concurrent elevation of counterregulatory hormones

• Occurrence

  • DKA: Type 1 diabetes

  • HHS: Type 2 diabetes

• Increasing incidence of both DKA and HHS in

same patient

• type 2 DM can also get DKA

DKA

Bottom line issue:

• absolute or relative insulin deficiency

• Far more frequent v HHS, BUT HHS has higher mortality

Triggers – more frequent:

• New onset diabetes

• Infection / acute illness

• Medication non – compliance

• Increase in counterregulatory hormones: glucagon,

cortisol, catecholamines, and growth hormone

what is DKA

glucose is really high, can’t move glucose into cells , can’t burn glucose since theres not enough insulin —> burn fat

DKA s/s

• exacerbated s/s of DM

• ABD pain

• hypotension

• altered LOC

• shock

• coma

• METABOLIC ACIDOSIS = CNS depression & CV collapse

• burn fat—> ketones (acidotic)

• Kussmual breathing (big deep and rapid breaths) to try and blow CO2 off

• fruity breath

• flushed dry skin

• 3 P’s

• BG usually >250 mg/dL

• HIGH ANION GAP acidosis (inadequate bicarb

• SEVERELY DEHYDRATED

how is DKA treated

insulin drip and fluids

three biochemical problems in DKA

• hyperglycemia

• ketonemia

• high anion gap metabolic acidosis

  • once pts BG is >200 will have glycosuria (glucose in urine) and will pull fluid pts become SEVERLY DEHYDRATED

DKA treatment

• regular insulin drip

• fluids

physiological changes in DKA

• Hyperglycemia due to increased glucose production and decreased utilization

• Osmotic diuresis and dehydration

• Hyperlipidemia due to increased lipolysis

• Metabolic acidosis/ketosis

• Altered potassium balance (increased from acidosis, will actually be LOW, from K+ shifting in cells, replace)

• Excess acids result in increased anion gap

• Altered consciousness related to acidosis and

dehydration

fluid and electrolytes changes in hyperglycemia emergencies (DKA and HHS)

• The clinical presentation of hyperglycemic

emergencies (DKA and HHS) is a product of

fluid volume losses related to osmotic diuresis

caused by hyperglycemia, ketosis (DKA), and

respiratory losses (DKA).

• Sodium, potassium, and phosphate losses may accompany fluid losses.

• K+ will initially be high, actually low need to correct and replace

• BUN and Cr elevated (secondary to dehydration)

• phosphate depletion (by insulin)

• mild hyponatremia

hyperglycemia is

greater than 250

causes:

• ↑ gluconeogenesis

• ↑ glycogenolysis

• ↓ glucose use by cells

• Glycogenolysis → 0 glycogen catabolized to lactic acid

ketonemia

elevated ketones= ketosis

• Decreased insulin availability →

• Decreased glucose transport into cells →

• Cellular “starvation” →

• Body uses other sources for energy

• Fat breakdown produces fatty acids →

• FA oxidized to ketones → ketonemia / ketosis

Ketones: β– hydroxybutyrate & acetoacetate

anion gap

evaluates bicarb

Difference of positive and negative ions

• Cations (+) and anions (-)

• Na+ ‒ (HCO3 ‒ + Cl ‒)

• Normal £ 12

• Elevated = metabolic acidosis

• sodium and chloride will stay about the same

• bicarb will be low

• anion is high

an anion gap that’s >12 is considered what

open

DKA BG

usually >200 can reach up to 600 mg/dL

Serum β– hydroxybutyric acid, acetone (ketones)

DKA ABG’s

• Mild: pH £ 7.3, HCO3‒ £ 15

• Severe: pH £ 7.0, HCO3‒ £ 10

DKA electrolytes

• K+: usually high, BUT NOT ALWAYS!

• Na+ and Cl‒ : low / normal

• CO2: low (normal 22 – 26)

DKA anion gap

• Mild: high end normal, 10 – 12

• Severe: above normal, > 12 (open)

why would we get a CBC with WBC and diff, UA, cultures in DKA

looking for infection

DKA diagnostics

• Cardiac monitoring, 12 lead EKG

• Chest x-ray

• Pneumonia

• Atelectasis

• KUB

• Free air

• Obstruction

• CT, MRI – possible,depending on initial findings

complications of DKA

• Hypoglycemia

• Hypokalemia

• Alkalosis

• Hypotension (dehydration)

• Aspiration / pneumonia

• Cerebral edema ( if corrected to fast)

• Sepsis / septic shock

difference with DKA and HHS

NO KETONES ARE PRODUCED

• can still move some glucose in the cells

• in nclex world more seen in Type 2 DM

HHS

• Hyperglycemia

• Dehydration

• Hyperosmolarity

• Incidence

  • Less than 1% of diabetic related hospitalizations

  • More common with Type II DM

  • BUT…mortality upwards of 15%

• More common in elderly, possible AMS

• Often develops over several days to weeks

• May have ketosis…if so, usually mild

sugar can get well over 600 mg/dL

HHS patho

• Decreased use of glucose and/or increased

production

• Hyperglycemia; increased extracellular

osmolality

• Osmotic diuresis

• Profound dehydration

• No ketoacidosis—hyperglycemia with

hyperosmolarity blocks lipolysis (this is the difference with DKA)

HHS etiology

• Inadequate insulin secretion, usually with type 2 diabetes

• Often in geriatric patients with decreased

compensatory mechanisms

• Stress response

meds

Affect blood glucose levels

• Thiazides

• Phenytoin (seizures)

• Glucocorticoids

• Beta blockers

• Calcium channel blockers

• Enteral and parenteral nutrition

HHS triggers

• infection

• new onset DM

• med noncompliance

HHS s/s

• early profound polyuria and polydipsia

• profound dehydration

• AMS

• comorbidities: HTN, thyroid, PSH

HHS glucose

can be around 800 mg/dL

HHS osmolarity

>320 mOsm/kg

blood has no water but LOTS of sugar

HHS electrolytes

• increased Na+

• increased glucose

• increased BUN

• increased Cr

• anion gap <12, wont be as acidic like DKA

HHS ABG

• pH >7.3

• HCO3- normal or slight elevation

HHS potential complications

Hypoglycemia

• Ensure glucose added to IV fluid appropriately

• Hypokalemia

  • Follow labs, replace as needed

• Hypervolemia

  • Clinical assessment, may need CVP monitoring

• Vomiting – aspiration

  • May need Salem sump to suction

• Cerebral edema

  • Avoid rapid drop in serum glucose

HHS

• blood sugar > DKA

• more “normal” ABG , no changes or little ones

• More electrolyte imbalances and renal

dysfunction

• Higher serum osmolarity than DKA

• Ketosis absent or mild

DKA & HHS interventions

Manage airway (DKA and HHS)

• Fluid replacement (DKA and HHS)

  • First use 0.9% NS, then 0.45% NS (1/2 NS)

  • Dextrose added when glucose approaches 200 mg/dL

• Monitor closely for signs of fluid volume overload and cerebral edema

DKA & HHS interventions

• Insulin therapy (DKA and HHS)

  • Fluid replacement initiate first; monitor K+

  • Loading dose (not in children)

  • Continuous infusion

  • Hourly glucose monitoring

• Decrease glucose by 50 to 75 mg/dL/hr

  • When glucose is less than 200 mg/dL, adjust infusion to maintain values of 150 to 200mg/dL (add dextrose)

DKA & HHS interventions continued

• Insulin therapy – transitioning to subcutaneous therapy

• Blood glucose < 200 mg/dL

two of the following criteria met to transition to SQ insulin

• Blood glucose < 200 mg/dL

• Two of the following criteria met (DKA):

  • pH > 7.30

  • HCO3 > 15 mEq/L

• Anion gap ≤ 12 mEq/L (closed)

• Ketosis must be resolved before transition (check urine and anion gap <12)

when do you give bicarb for DKA

ONLY if pH is <7.0 (less than)

changing to SQ therapy

• Basal/bolus insulin regimen preferred

  • Long-acting/short- or rapid-acting insulin

  • Insulin pump

• Administer subcutaneous insulin prior to

discontinuing IV insulin with attention to insulin

action profile

• Monitor at least every 6 to 8 hours

  • Determined by meal schedule

  • If NPO, then every 6 hours

what do we want to keep the K+ at for DHA & HHS

4-5 mEq/L

• establish renal function first

HYPOglycemia lab level

less than 70 mg/dL

hypoglycemia etiology

Excess insulin/oral agents

• Alcohol potentiates hypoglycemic effects

• Insufficient nutrition intake

• Excess exercise

• Medications (e.g., beta blockers)

• Renal impairment

• Diabetic neuropathy

  • Hypoglycemia unawareness

  • gastroparesis

hypoglycemia assessment

Rapid decrease in serum glucose levels

• Activation of sympathetic nervous system

(epinephrine release)

• Tachycardia

• Diaphoresis

• Pallor

• Dilated pupils!!!!!

• lightheaded

• Hypoglycemia unawareness

neuro affects with low BG

• Restlessness

• Difficulty thinking and speaking

• Visual disturbances

• Paresthesias

• Change in LOC

hypoglycemia interventions

• 15 g carbohydrate orally (carbs + protein,like pb&j, cheese )

• 50% dextrose (EMS, ED, ICU settings)

• Glucagon

• Oral glucose

• Assess response: should improve rapidly

• Adjust insulin regimen temporarily

• Prevention and teaching

Diabetes Insipidus (DI)

not releasing adequate ADH —> PEE TOO MUCH—> CAN DIE FROM DEHYDRATION

DI patho

deficiency in synthesis or release of ADH

• excessive WATER LOSS

• dehydrated and hypotensive —> HYPOVOLEMIC SHOCK

what are the types of DI

• neurogenic (central)

• nephrogenic (kidney)

neurogenic DI

• more common

• ADH deficiency

• brain not producing ADH —> pituitary swelling, tumor, trauma)

nephrogenic DI

• kidneys are insensitive to ADH

• dont respond

ADH disorders

• DI

• SIADH (TOO MUCH ADH)

DI neurogenic etiology

• genetically predisposed

• head trauma

• neurological abnormalities

  • increased ICP

• pituitary surgery

DI nephrogenic etiology

• genetically predisposed

• chronic renal disease

• multisystem disorders affecting the kidneys

  • multiple myeloma

  • sickle cell

  • cystic fibrosis

DI nephrogenic etiology drugs

• ethanol

• phenytoin (dilantin)

• lithium

• demeclocycline

• amphotericin

• methoxyflurane (inhaled anesthetic)

DI assessment

PEE A LOT, high urine output

• Thirst and polydipsia

• Hypotension

• Decreased skin turgor

• Dry mucous membranes

• Tachycardia

• Weight loss

• Low right atrial pressure/central venous pressure (RAP/CVP) and pulmonary artery (PA) pressure

• Neurological changes

  • Hypernatremia and hypovolemia (DRY IS HIGH )

• DI= dry inside

DI dx

urine sample

• Dilute urine with low specific gravity (OVERLOADED, LOTS OF FLUID)

• Increased serum osmolality (blood concentrated)

• Increased blood urea nitrogen (BUN) and

creatinine

• Hypokalemia or hypercalcemia

• Water deprivation test

• Vasopressin test (to differentiate)

what does the vasopressin test do

to differentiate betweeen neurogenic and nephrogenic

• will give vasopressin, if they STOP PEEING, it is central/NEUROGENIC—> the body finally gets ADH which is vasopressin and they stop peeing as much and and urine becomes more concentrated —> increased specific gravity

• if we give ADH and the pt doesn’t respond and keeps peeing, no change in UO, urine stays diluted

how does the sodium look in DI

WILL BE HIGH

• HIGH and DRY

• >145 mEq/L

• Free water loss due to

  absent or diminished

  release of ADH or lack of

  response by the kidneys

  results in

  hemoconcentration of

  sodium DRY IS HIGHHHHHH

osmolality in DI

>295

• Free water loss due to

  absent or diminished

  release of ADH or lack of

  response by the kidneys

  increases serum osmolality;

  will be normal in secondary

  DI

urine osmolality in DI

<100

Free water loss into urine

decreases urine osmolality

DI interventions

VOLUME REPLACEMENT

• Monitor for fluid overload and water intoxication once therapy has been initiated

• Hormone replacement

  • Vasopressin (desmopressin)

• Thiazide diuretics (nephrogenic)

pt education of DI

Pathogenesis of DI

• Dose, side effects, and rationale for prescribed medications

• Parameters for notifying the physician

• Importance of adherence to medication regimen

• Importance of recording daily weight measurements to identify weight gain

• Importance of wearing a Medic-Alert identification bracelet

• Importance of drinking according to thirst and

avoiding excess drinking

SIADH- syndrome of inappropriate antidiuretic hormone

THEY ARE NOT PEEING ENOUGH

• EXCESS ADH (withholding water)

• plasma hypotonicity (hold onto fluid, become overloaded)

SIADH can be from

• CNS disease

  • trauma

  • tumor

• Malignancy (tumors produce, decreased ADH)

  • small lung cell carcinoma

  • hodgkin’s lymphoma

  • pancreatic and duodenal carcinoma

• Pulmonary disorders

  • TB, lung abscess, PNA, COPD

what meds can cause SIADH

• SSRI

• TCA

• Antiepileptics—> carbamazepine, valporic acid

• Chemo —> cyclophosphamide

SIADH CNS s/s

• low Na+

• confusion

• headache

• seizures

• weakness

SIADH pulmonary system

• increased RR

• dyspnea

• adventitious lung sounds

SIADH CV s/s

• HTN

• elevated CVP and PA pressure (overloaded)

• edema

SIADH GI system s/s

• anorexia

• N/V

• muscle cramps

• decreased bowel sounds

SIADH labs

• hyponatremia (overloaded, hemodilutional)

• decreased serum osmolality (overloaded)

• high urine sodium

• concentrated urine

• decreased BUN and CR (overloaded)

• decreased albumin

sodium in SIADH

<135 mEq/L (diluted)

• free water retention due to over secretion of ADH —> dilutes Na+ , holding onto water/urine and the remaining Na+ gets diluted

osmolality serum in SIADH

<280

free water RETENTION due to over secretion of ADH , decreases osmolality from overload