LEFORT FRACTURES

ARTERIAL LINE WAVEFORM

RULE OF 9’S

12 LEAD EKG

SUBDURAL HEMATOMA

1) No clear delineation

2) Blood between dura and arachnoid layers

3) Usually venous in nature

4) Increased morbidity and mortality rate

a) Increases with every millimeter of brain tissue shift

5) Types

a) Acute

i) Onset within 24 hours

b) Subacute

i) Onset within 2-10 days

c) Chronic

i) Onset after 2 weeks

6) Elderly

a) Larger bleed with slowly developing symptoms due to cerebral atrophy

7) Younger person

a) Rapid onset with marked increased ICP

8) Pediatric

a) Generally occur in children < 18 months

b) Fontanelle not fully closed

c) Ssx

i) Bulging fontanelle

ii) Separation of sutures

iii) Shock

iv) Retinal hemorrhage

v) Die from bleeding to death

EPIDURAL HEMATOMA

1) Clear line of delineation

2) Lens shaped

3) Bleeding between skull and dura mater

4) Usually arterial but can be venous

5) Laceration of middle meningeal artery in temporal lobe area

6) Classic symptomology

a) Transient loss of consciousness followed by period of lucidity then decreased level of consciousness

i) Hit head

ii) Lose consciousness

iii) Regain consciousness

iv) Loss of consciousness

7) Uncal herniation

a) Will result in dilation of ipsilateral pupil with contralateral neuro deficits and posturing

8) Classification

a) Acute

i) Usually arterial bleed

ii) Onset of symptoms within a few hours

b) Subacute

i) Usually venous bleed

ii) Takes longer time for onset of symptoms

SUBARACHNOID HEMORRHAGE

1) Bleeding between arachnoid mater and pia mater

2) Trauma most common cause

3) May occur with other injuries or as only evidence of trauma

a) Rupture of aneurysm in Circle of Willis

i) Berry aneurysm rupture

b) Maintain ICP, CPP, etc

4) Aneurysmal SAH

a) Medical

b) Rupture may be self-limiting

i) 2nd rupture is 100% mortality

c) Quick loss of consciousness then dies

d) Fatal within short period of time

e) Worse headache ever

i) Die in emergency department or drop dead

f) Managed differently than all others

i) Decrease amount of perfusion to control blood pressure to prevent increased pressure

ii) Decrease heart rate

iii) Cardene

iv) Nipride

v) SPB < 140

5) Ssx

a) Presents similar to meningitis

b) Severe headache

i) Worst ever

ii) Deteriorate rapidly

c) Vomiting

d) Stiff neck

i) Bending down hurts

e) Leg pain

i) Drawing up hurts

f) Confusion

g) Lethargy

h) Loss of consciousness

i) Blood accumulates in meninges

6) Avoid lumbar puncture due to possibility of uncal herniation until CT scan verifies SAH vs meningitis

GRAVE’S DISEASE AND THYROTOXICOSIS

1) Thyroid storm

2) Autoimmune disease which causes overstimulation of TSH receptors

a) Thin hair

b) Papery skin

c) Bulging eyes

d) Hypermetabolic

3) Causes

a) Iodine

i) Amiodarone

b) Infection

c) Surgery to thyroid

d) Toxemia

4) Presentation

a) Dramatic weight loss

b) Chest pain

i) Palpitations

ii) SOB

iii) Trying to keep up with metabolic demand leading to increased cardiac output

c) Fever

d) Tremors

e) Nervousness

f) Marked tachycardia

g) Hypertension

h) Profuse sweating

5) Treatment

a) Antipyretics

i) NO ASA

b) Supportive care

c) LOTS of fluids

d) Correct electrolytes

e) Supplemental oxygen

f) Beta-blockers

i) Cardioprotective

g) PTU or MMI

i) PO

ii) NGT

h) Consider IV glucocorticoids

i) Decadron inhibits hormone production and conversion from T4 to T3

(1) Actual metabolite that causes cells to “ramp up”

MYXEDEMA COMA AND HYPOTHYROIDISM

1) Causes

a) Infection

b) Cessation of thyroid replacement

c) Thyroid removal

2) Presentation

a) Primarily women

b) Almost exclusively over 60

c) >90% of cases occur in winter

d) Fatigue

e) Weight gain

f) Cold intolerance

g) Deep voice

h) Coarse hair

i) Obese

j) Round face

k) Slow appearance

l) Officially “myxedema coma” with any change in level of consciousness

i) Hypometabolic

3) Treatment

a) Supportive during comatose states

b) IV levothyroxine

i) T4

c) Triostat

i) T3

d) Adrenal insufficiency

i) DO NOT GIVE Etomidate

(1) Can potentiate adrenal insufficiency

ADDISON’S DISEASE/ADRENAL INSUFFICIENCY

1) Causes

a) Autoimmune disease

i) Primary Addison’s

b) Decreased levels of ACTH

i) Secondary Addison’s

c) Acute withdrawal from glucocorticoid therapy

i) Prednisone

2) Presentation

a) Weakness

b) Weight loss

c) Fatigue

d) Decreased blood pressure

e) Negative ACTH test

i) No increase in serum cortisol with ACTH administration

3) Treatment

a) Supportive care

b) ABCs

c) Volume replacement

d) Correct electrolytes

e) Hydrocortisone or Decadron

f) NO Etomidate

CUSHING’S SYNDROME/HYPERALDOSTERONISM

1) Causes

a) Chronic glucocorticoid use

b) Pituitary disorder

c) Oat cell carcinoma

d) Adrenal carcinoma

2) Presentation

a) Upper body obesity with thin arms and legs

b) Rounded face

c) “Buffalo hump” on back of neck

d) Fatigue

e) Hypertension

f) Hyperglycemia

g) Facial hair on women

3) Treatment

a) Initiation or reduction of glucocorticoids

i) Causes negative feedback loop

ii) Causes adrenals to decrease production of glucocorticoids

b) Support symptoms

c) Surgery to remove some of adrenal gland

SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH)

1) Released by posterior pituitary

a) Tells kidneys to hold onto water

2) LOTS of ADH produced

a) Kidneys hold excessive water

b) Not excreting water at same rate of other chemicals

i) Blood hyperosmolar

3) Causes

a) Oat cell carcinoma

b) Viral pneumonia

c) Head injury

i) CVA

ii) ICH

4) Presentation

a) Neuro changes

i) Confusion

ii) Coma

b) Cerebral edema

i) Increased ICP

c) Seizures

d) Hyponatremia

e) Urine osmolarity/specific gravity

i) Concentrated

5) Treatment

a) Restrict fluids

i) Over fluid loaded

b) Diuresis

i) Push water out of kidneys

ii) Lasix

c) Hypertonic saline

i) Treat slowly

ii) Do not raise sodium more than 0.5 mEq/liter/hr

DIABETES INSIPIDUS

1) No ADH being released or used

2) Causes

a) Head injury

i) ICH

ii) CVA

b) Dilantin toxicity

3) Presentation

a) Extreme urine output with very low urine osmolality/specific gravity

i) Looks like free water

(1) Clear

ii) Copious amounts

4) Treatment

a) Aggressive fluid resuscitation

b) Vasopressin

i) Cardiovascular effects

ii) Exogenous ADH

c) Desmopressin

i) DDAVP

ii) Does not have vasoconstricting effects of Vasopressin

ABG INTERPRETATION

Respiratory

Opposite

Metabolic

Equal

pH: 7.35-7.45

CO2: 35-45

HCO3: 22-26

Respiratory acidosis: pH < 7.35, CO2 > 45

Respiratory alkalosis: pH > 7.45, CO2 < 35

Metabolic acidosis: pH < 7.35, HCO3 < 22

Metabolic alkalosis: pH > 7.45, HCO3 > 26

CUSHING’S TRIAD—EMMINENT UNCAL HERNIATION

ANTIDOTES FOR SELECT POISONING

Carbon monoxide 1) Oxygen: 100% for 2-6 hrs; competes with CO; causes positive neurological change

2) Hyperbarics: do NOT use if lactic acidosis present; tachycardia, hypotension, use if patient can wait 4-6 hours

Cyanide 1) Amyl or sodium nitrate2) Nathiosulfate

Organophosphates/organocarbamatos 1) Atropine2) 2-PAM

Methemoglobinemia 1) Methylene blue

Anticholinergic 1) Physostigmine

Coumadin 1) Vitamin K

Heparin 1) Protamine

Beta-blockers 1) Glucagon

Calcium channel blockers 1) Calcium

BECK’S TRIAD—PERICARDIAL TAMPONADE

COPD VS ASTHMA

SHOCK

PLACENTAL PLACEMENT

Abruption: painful, dark red blood

Previa: painless, bright red blood

SPINAL CORD INJURIES