-
Describe the dosing of insulin in DKA
- 0.1 u/kg Bolus
- Followed by drip at 0.1 u/kg/hr
-
What is the max drop in BGL per hour in the treatment of DKA?
100 mg/dl
-
Once BGL = 300 what is added to the insulin drip?
D5W
-
What is the central health issue in HHNK?
Too much sugar compared to their insulin production
-
Describe the presentation of HHNK
- SEVERE dehydration
- Absence of ketosis – NO kussmaul breathing
- Relative hypernatremia
- Hyperglycemia [> 800 mg/dl common]Elevated BUN/Creatinine ratio
-
Describe the treatment of HHNK
AGGRESSIVE fluid rehydrationInsulinAnticipate severe hypokalemia
-
What are the causes of Diabetes Insipidus (DI)?
-
Describe the presentation of Diabetes Insipidus (DI)
- Extreme urine output w/very low urine osmolarity/specific gravity
- Hypernatremia
-
Describe the treatment of Diabetes Insipidus
- Aggressive fluid replacement
- vasopressin (Pitressin©)dDAVP (DDAVP©, Stimate©, Minirin©)
-
Describe the condition of Syndrome of Inappropriate ADH (SIADH)
A syndrome of increased ADH activity despite reduced plasma osmolarity
-
Describe the presentation of Syndrome of Inappropriate ADH
- Dilutional hyponatremia
- Cerebral edema
- Seizures
- Urine osmolarity/Specific gravity elevated
-
Describe the treatment of Syndrom of Inappropriate ADH (SIADH)
- Restrict fluids
- Diuresis
- 1° loop diuretics
- Democlocycline (tetracycline family)
- ADH receptor antagonism
-
Describe the treatment of GI hemorrhage
- Essentially treat as a trauma pt
- Also NGT/OGT & evacuate stomach
- octreotide (Sandostatin) 25-50 mcg IVP followed by 25-50 mcg/hr IVgtt - Reduces hepatic portal pressures, allows relief of venous congestion
- vasopressin (caution in CAD) - Decreases arterial pressure feeding to the hepatic portal system
-
Describe the presentation of Graves Disease
- Dramatic weight loss
- CP, SOB & palpitations
- Fever
- Tremor, nervousness
- Marked tachycardia (AF common)
- ** Any new tach/AF in an otherwise healthy female **
-
Describe the treatment of Graves Disease
- Antithyroid meds needed
- Antipyretics (Avoid ASA)
- Fluids
- Correct electrolytes: K+, Mg+
- Supplement O2 delivery
- Consider IV glucocorticoids, dexamethasone specifically inhibits hormone production & conversion from T4 to T3
- Tachycardias not likely to respond to digitalis, will convert once antithyroid therapy initiated
-
Describe the presentation of Myxedema Coma / Hypothyroidism
- Primarily women
- Almost exclusively > 60 YOA
- > 90% of cases occur in winter
- Fatigue & weight gain
- Cold intolerance, deep voice, coarse hair
- Officially “myxedema coma” upon any change in LOC
-
Describe the treatment of Myxedema Coma / Hypothyroidism
- Supportive during comatose states
- IV levothyroxine (T4)
- Watch for adrenal insufficiency (Etomidate issues)
-
Describe the presentation of Addison's Disease / Adrenal Insufficiency
- Inadequate aldosterone, cortisol & androgens
- Fatigue, weakness, low BP 2°
- ↓ Na+/H2O retention
- Hypoglycemia
- Poor catecholamine production
- Failure to respond to exogenous pressor agents
-
Describe the treatment of Addison's Disease / Adrenal Insufficiency
- Avoid abrupt discontinuation of chronic glucocorticoid use
- May need to initiate steroids
- Caution w/Etomidate (overstated)
-
What are the causes of Cushing's disease?
- Chronic glucocorticoid use w/abrupt cessation
- Pituitary disorders (too much ACTH released
- Oat Cell carcinoma (‘fake’ cortisol)
- Adrenal carcinoma (too much cortisol produced/secreted)
-
Describe the presentation of Cushing's disease
- Upper body obesity w/thin arms & legs (muscle wasting)
- Rounded face “buffalo hump”
- Fatigue, HTN, hyperglycemia
- Incr. Norepinephrine/Epi
- Fatty & amino acids convert to glucose
- Type II DM (hyperglycemia wears out the pancreas)
-
Describe the treatment for Cushing's disease
- Initiation or reduction of glucocorticoids (Hydrocortisone)
- Supportive
- Need surgery
-
What are the causes of pancreatitis?
- EtOH abuse
- Biliary stone disease
- Steroids & antibiotics
- Infections (viral/bacterial)
-
Describe the presentation of pancreatitis
- Low Ca+
- Elevation of the left diaphragm w/left base atelectasis
- Bilateral pleural effusions
- Concomitant sepsis & ARDS
- Renal failure
- Cullen’s sign
-
Describe the treatment of pancreatitis
- Fluid resuscitation
- NPO & place NGT/OGT
- Meperidine vs. Morphine (Sphincter of Oddi spasticity)
- Alternate use of atropine, β-blockers, Narcan® & tetrodotoxin
- Anticipate progression
- Sepsis
- ARDS
- MODS
- DIC
- DEAD
- Abx for sepsis (Rocephin, Ampicillin)
-
What causes bowel obstructions?
- Post operative adhesions
- Malignancy
- Crohn’s disease
- Hernias
-
Desccribe the presentation of bowel obstructions
- Large vs. Small
- Bowel ischemia results in sepsis
- Pancreatitis is common
-
Describe the treatment of bowel obstruction
- NPO & place OGT/NGT
- Aggressive fluid resuscitation
- Aggressive pain control
- Antiemetics
- Antibiotics
- Ancef
-
What are the primary issues with cirrhosis &/or hepatitis?
- Ammonia toxicity
- By-product of protein metabolism
- TPN, blood, etc… Amine removal from amino acid
- NH3 converted to urea & glutamine for renal excretion
- Hypokalemia
- Diuretics
- Diarrhea
- Alkalotic states
-
Describe the presentation of hepatic encephalopathy 2° to cirrhosis &/or hepatitis
- ⇧ AST & ALT (SGOT/SPGT)
- ⇧ BUN
- Stuperous ⇨ obtunded ⇨ coma
- “Coarse muscle flapping”
-
Describe the treatment of hepatic encephalopathy 2° to cirrhosis &/or hepatitis
- Stop GI bleeding & evacuate bowel of blood w/OGT/NGT
- STOP protein intake (TPN, etc.)
- Correct K+ levels
- Stop K+ retention
-
What causes splenic rupture?
Trauma - most commonly affected organ in blunt force trauma
-
How does splenic rupture present?
- Left shoulder pain (referred pain AKA Kehr’s sign)
- Shock
-
Describe the treatment of splenic rupture
- Supportive
- Aggressive fluid resuscitation & PRBCs
- Get to surgeon
-
Describe Brudzinski's sign & it's significance
- Meningitis
- Flex the neck & pt will bring up hamstring
-
Describe Kernig's sign & it's significance
- Meningitis
- Bring up the pt's hamstring & the pt will flex their neck
-
Describe Cullen's sign & it's significance
- Pancreatitis
- Periumbilical bruising
-
Describe Grey-Turners sign & it's significance
- Pancreatitis
- Flank & groin bruising
-
Describe Kehr's sign & it's significance
- Splenic disease/rupture
- Left shoulder referred pain
-
Describe Murphy's sign & it's significance
- Gallbladder
- RUQ & push up, have pt take deep breath
- + sign = pain & inability to take a full breath
-
Describe Levine's sign & it's significance
- Cardiac pain
- Clenched fist over chest
-
Describe the body's response to cold
- Peripheral vasoconstriction
- Skeletal muscle vasodilation
- ⇧ Cardiac Output
- Shivering
- Increases MRO2 by up to 600%
- Limited by available glycogen stores
- Loss of shivering @ 32°C (89.6° F)
-
At what temperature does shivering stop?
32° C (89.6° F)
-
Describe the physiologic response to hypothermia
- Initially metabolism⇧to produce heat
- Metabolism ⇩ by ½ for every drop in core temp of 10° C
- Pts BGL will ⇩ with mild chronic hypothermia
- BGL is ⇧ w/severe hypothermia as insulin stops working
- Respiratory minute volume (VE) ⇩
RR becomes inadequate to blow off CO2 - respiratory acidosis follows⇩ CO⇧ SVR Capillary leak decreases intravascular volumeMetabolic acidosis related to anaerobic metabolismEnzyme function ⇩ dramatically- Coagulation deficits
- Medication biometabolism deficits
-
Describe mild hypothermia
- >32-34°C
- ⇧BMR, CO, HR begins to ⇩ @ 32° C
-
Describe moderate hypothermia
- 29 - < 32° C
- Body stops attempting to conserve or produce heat @ 32° C, shivering stops, LOC & SVR fall, acidosis, hyperglycemia, CO falls
-
Describe severe hypothermia
- < - 28° C
- Hypotension
- ECG Δ: Prolonged QR, QRS, QT intervals, VF
- risk highest @ 22° C. Osborn waves clear @ 25° C.
- PT, PTT ⇧by 50%, Platelets ⇩ by 40%
-
-
Describe the treatment of hypothermia
- Remove from cold & wet environment
- Manage airway, consider ETI, Risk of VF
- Handle gently
- Only start CPR if monitor shows VF or asystole
- Defer meds until core temp > 30° C
- < 33° C we see enzymatic retardation
-
How do you accomplish passive external re-warming?
Pt allowed to re-warm self w/blankets & transport vehicle heater
-
What comprises active external re-warming?
- Heat placed on external body surfaces (neck, groin, axilla)
- Watch for afterdrop
-
What comprises active internal re-warming?
- Heat directly to core
- IVF, hemodialysis, gastric lavage, rectal lavage, ECMO
-
Describe the neuro complications from hyperthermia
Cerebral edema & seizure activity 2° to hyponatremia
-
Describe the renal complications from hyperthermia
Hypokalemia, ATN
-
Describe the hepatic complications from hyperthermia
Hypoglycemia & ⇧ clotting times
-
Describe the muscular complications from hyperthermia
Increased CK (CK-MM) & rhabdomyolosis
-
Hyperthermia can also cause what conditions 2° lysosomal enzymes?
-
Where & under what conditions do heat cramps occur?
- In heavily exercised muscles
- High heat
-
What causes heat cramps?
- Hyponatremia
- Associated w/only H2O replacement
-
Describe the treatment of heat cramps
- Cool
- Rehydrate w/Salt containing solutions (0.9% saline)
-
Define Heat Exhaustion
Defined as an increase in core temp w/o neurologic impairment
-
Describe Heat Exhaustion
- Temperature is lower & symptoms less severe than heat STROKE
- Pt retains ability to sweat
-
Describe the treatment of Heat Exhaustion
- Cooling
- Fluid replacement
- Electrolyte replacement
-
What is Heatstroke?
A life threatening emergency characterized by failure of the body to dissipate heat effectively
-
Describe Heatstroke
- LOC is altered
- Core temp ⇧ 42° C
- O2 demand exceeds supply
- Respiratory alkalosis ⇨ Metabolic acidosis
- High output cardiac failure (use caution w/over-aggressive cooling)
-
Describe the treatment of heatstroke
- Aggressive cooling
- Soak & air flow (Conduct/Convect)
- Aggressive airway management
- Don’t under ventilate, use vent to reduce work load (use of AC mode ideal &/or pressure support)
- Expose
- IV fluids
- Prevent shivering
- Phenothiazines & NMBAs
- MRO2 ⇧ x 600% w/shivering!Place OGT/NGT & consider H2 blockers
- cimetidine (Tagamet®) * consider drug interactions
- Foley & monitor
- Volume output
- Color/evidence of rhabdomyolosis
- Monitor labs
- ABGs for acidosis
- Watch clotting factors for early onset DIC
- Monitor liver enzymes
- Watch Na+ for hyponatremia
-
Describe the treatment of rhabdomylosis in heat related illness
- ⇧ urine output to 2 mL/kg/hr
- Alkalinize urine w/NaHCO3-
- Assist diuresis w/Lasix &/or mannitol
-
Describe the treatment of hyponatremia in heat related illness
Replace by correcting Na+: 3.3% saline SLOWLY (central pontine myelinolysis)
-
Describe the pathophysiology & presentation of TCA intoxication
- Mimics Class I AAs (quinidine, lidocaine)
- Blocks Na+ Channels
- Inhibits NE (norepinephrine) uptake [Like
- cocaine]
- Blocks PNS (Peripheral Nervous System) [Like jimson weed]
- Early tachycardia
- Widening of QRS
- Aberrant SVT
- Torsades de Pointes/VT/VF
-
Describe the treatment of TCA intoxication
- NaHCO3-
- Norepinephrine: 1st choice pressor
- Dialysis NOT helpful
-
Identify the common cardioselective beta blockers
- atenolol (Tenormin®),
- metoprolol (Lopressor®),
- esmolol (Brevibloc®),
- betaxolol (Betoptic®)
-
Identify the common non-cardioselective beta blockers
- propanolol (Inderal®),
- sotalol (Betapace®),
- nadolol (Corgard®),
- timolol (Timoptic®)
-
Describe the presentation of a cardioselective β blocker OD
- Bradycardias w/resultant hypotension
- Look for escape rhythms
-
Describe the potentials issues w/the use of Epi in the treatment of β-blocker OD
- May result in an “Inverse Epinephrine Response”
- With β1 blocked, Epi can only stimulate β2 & α1 β2 will vasodilate
- May attenuate α1 effect
- May override α1 completely ⇨ hypotension
- α1 will vasoconstrict ⇨ ⇧ BP ⇨ baroreceptors triggered ⇨ ⇩ HR = BAD
-
Describe the presentation of a Non-cardioselective β blocker OD
- Respiratory distress, exacerbation of RAD
- Beta2 blocked @ same time as Beta1
- Inhibits bronchodilation
-
Describe the treatment of Beta-blocker OD
- Atropine rule out / Parasympathetic tone/prasympathetic tone prophylaxis (will pay off post TCP capture)
- TCP ASAP
- Glucagon 2-5 mg IVP (incr. cAMP via glucagon receptor)
- dopamine (Intropin) PRN for hypotension
-
Describe the presentation of Cardiospecific Ca+ Channel Blocker OD
- Severe bradycardias
- AV Dissociation w/comcomitant hypotension
-
Describe the presentation of Vasculomotor specific Ca+ Channel Blocker OD
Severe hypotension
-
Describe the treatment of Cardiospecific Ca+ Channel Blocker OD
- CaCl/Ca+ Gluconate
- TCP
- Maintain Insulin Euglycemia
-
Describe the treatment of Vasculomotor specific Ca+ Channel Blocker OD
- CaCl/Ca+ Gluconate
- TCP
- Maintain Insulin Euglycemia
-
Describe the presentation of Digitalis toxicity
- Visual disturbances {Yellow/Green Halos}
- Bradycardia, SVT, VT, AV Blocks
-
Describe the treatment of Digitalis toxicity
- Digoxin Immune Fab (Digibind)
- Assure normal electroclytes
- K+ 1st, then Ca++ & Mg++
- TCP
- lidocaine (Xylocaine), MagSulfate & phenytoin (Dilantin) for tachyarrhythmias
- Caution w/electricty
-
Describe the presentation of hyperkalemia
- Profound acidosis (DKA, vent mismanagement, etc)
- K+ supplement OD
- ECG: Flattening/slurring of P's w/peaked T's
-
Describe the treatment of hyperkalemia
- CaCl
- Raises the action potential threshold to compensate for hyperkalemic elevated resting potential
- CAUTION w/hyperkalemia secondary to malignant hyperthermia
- NaHCO3- [Do not mix w/CaCl]
- Insulin
- D50
- Beta2 agonists
- sodium polystyrene sulfonate (Kayexalate)
- furosemide (Lasix)
-
Describe the presentation of hypokalemia (< 3.5)
- Loop diuretic misuse/OD
- Serum K+ important as well as pH
- ECG: Peaked P's, flattened/slurred T's & apperance of U's
-
Describe the treatment of hypokalemia
- KCl, KPhos
- Commonly 10-20 mEq/hr (10 mEq/hr peripheral, 20- central)
- Never more than 0.5-1.0 mEq/kg/hr
-
Describe the presentation of mild ASA intoxication
- Tinnitus
- Headache
- Vertigo
- Mental confusion
- Thirst
- Sweating
- N/V
- Hyperventilation
-
Describe the presentation of severe ASA intoxication
- Agitation/restlessness
- Coma
- Seizures
- Non-cardiac pulmonary edema
- Electrolyte disturbances (TCO2, HCO3-)
-
Describe the treatment of ASA poisoning
- Gastric emptying
- Charcoal
- Alkaline diuresis using NaHCO3-
- Ion trapping mechanism
- Hemodialysis
- Management of Acid/Base & electrolyte disturbances
-
Describe the presentation of acetaminophen (APAP) intoxication during Stage I
- "Flu like symptoms"
- Occurs w/in 30 min - 24 hrs
- N/V/Anorexia
- Malaise
- Pallor
- Diaphoresis
-
Describe the presentation of acetaminophen (APAP) intoxication during Stage II
- "Ow my liver!"
- 24 - 48 hrs
- RUQ pain/tenderness
- Incr Liver enzymes
- Incr serum bilirubin
- Incr PT
- Oliguria as a result of ATN
-
Describe the presentation of acetaminophen (APAP) intoxication during Stage III
- "Gonna die now"
- 72-96 hrs
- Peak for liver function abnormalities
- Return of anorexia, N/V, Malaise
- Jaundice becomes apparent
- Hepatic encephalopathy
- DIC
- Death d/t fulminant hepatic necrosis
-
Describe the presentation of acetaminophen (APAP) intoxication during Stage IV
- "I'm not dead yet"
- 4 days to 2 wks
- Resolution period
- Liver functions return to normal baseline values
- Patients are asymptomatic
-
What is a toxic level of acetaminophen poisoning?
7.5 GM or 150 mg/kg
-
How long post ingestion do you obtain serum levels in acetaminophen poisoning?
4 hrs
-
What is the treatment for acetaminophen poisoning?
- n-acetylcysteine (Mucomyst)
- Orally 140 mg/kg followed by 70 mg/kg Q 4 hrs for 17 dosings
-
Describe the presentation of ethylene glycol / methanol poisoning
- Profound anion gap
- Osmolar gap
- Nystagmus / blindness
- Depressed DTRs
- Stupor/Coma/Convulsions
- Myoclonic jerks
- Hypothermia/Low grade fever
- Profound hypocalcemia
-
Describe the treatment of ethylene glycol / methanol poisoning
- IV ethanol drip
- fomepizole (Antizol)
- Thiamine
- pyridoxine (Aminoxin)
-
What are the treatment PEARLS for cocaine use?
- Avoid beta-blockers
- Utilize alpha-blockers for HTN
- Use benzodiazipines for anxiety
-
Identify a caution for treatment of the pt exposed to hallucinogens
Beware of violent propensity
-
What treatment may be required for alcohol intoxication?
Dialysis
-
What is the reversal agent & dosing schedcule for benzodiazepines?
- 0.1 - 0.2 mg IVP, Max 3.0 - 5.0 mg
- Caution w/Seizure or chronic use history
-
What is the reversal agent and dosing schedule for opioids?
- 0.4 - 2.0 mg IVP, Repeat PRN
- Reverses all beneficial effects of opioids as well as problematic
- Be alert for negative pressure induced pulmonary edema
-
What is the treatment paradigm for Carbon Monoxide (CO) poisoning?
-
What is the treatment paradigm for Organophosphate (OGP)/Organocarbamate exposure?
-
What is the treatment paradigm for Methemoglobinemia?
methylene blue
-
Describe the presentation of anticholinergic crisis
- Mad as a Hatter
- Red as a Beet
- Dry as a Bone
- Blind as a Bat
-
What is the treatment paradigm for anticholinergic crisis?
physostigmine (Eserine)
-
What is the mechanism of action for physostigmine in anticholinergic crisis?
Inhibits acetylcholinesterase
-
What is the treatment paradigm for coumadin poisoning?
- Vitamin K (IV, IM)
- 6 hr onset
- High rate of anaphylaxis when given IVP
- FFP - for when 6 hrs is too long
-
What is the treatment paradigm for heparin OD?
- Protamine
- Derived from whale sperm so watch for allergies to seafood & fish
- Typical profile is to give a small test dose then give larger dose once risk of anaphylaxis is deemed low
-
What is the treatment paradigm for Beta & Calcium channel blockers?
-
Where is CSF created?
The Choroid Plexus
-
Where is CSF reabsorbed?
Arachnoid Villi
-
What is the name of the thin cerebral cortex cover?
Pia Mater
-
What is the name of the tough outer covering?
Dura Mater
-
Where is CSF located?
Subarachnoid space
-
What is the significance of the finding on CT that a brain hemorrhage is lenticular in shape?
Diagnostic for epidural bleed
-
What is Cranial Nerve I?
Olfactory
-
What is Cranial Nerve II?
Optic
-
What is Cranial Nerve III?
Oculomotor
-
What is Cranial Nerve IV?
Trochlear
-
What is Cranial Nerve V?
Trigeminal
-
What is Cranial Nerve VI?
Abducens
-
What is Cranial Nerve VII?
Facial
-
What is Cranial Nerve VIII?
Vestibulocochlear
-
What is Cranial Nerve IX?
Glossopharyngeal
-
What is Cranial Nerve X?
Vagus
-
What is Cranial Nerve XI?
Accessory
-
What is Cranial Nerve XII?
Hypoglossal
-
What does the Olfactory Cranial Nerve control?
Also classify as Sensory, Motor or Both
-
What does the Optic Cranial Nerve control?
Also classify as Sensory, Motor or Both
-
What does the Oculomotor Cranial Nerve control?
Also classify as Sensory, Motor or Both
- Eye movement [Adduction]
- Motor
-
What does the Trochlear Cranial Nerve control?
Also classify as Sensory, Motor or Both
-
What does the Trigeminal Cranial Nerve control?
Also classify as Sensory, Motor or Both
- Facial sensory, chewing
- Both
-
What does the Abducens Cranial Nerve control?
Also classify as Sensory, Motor or Both
- Eye movement [Abduction]
- Motor
-
What does the Facial Cranial Nerve control?
Also classify as Sensory, Motor or Both
- Facial muscles, taste
- Both
-
What does the Vestibulocochlear Cranial Nerve control?
Also classify as Sensory, Motor or Both
- Balance / Position
- Sensory
-
What does the Glossopharyngeal Cranial Nerve control?
Also classify as Sensory, Motor or Both
-
What does the Vagus Cranial Nerve control?
Also classify as Sensory, Motor or Both
- Parasympathetic Nervous System (PNS), Motor of Larynx/Pharynx
- Both
-
What does the Accessory Cranial Nerve control?
Also classify as Sensory, Motor or Both
- Shoulder / Head movement
- Motor
-
What does the Hypoglossal Cranial Nerve control?
Also classify as Sensory, Motor or Both
-
What is the formula to calculate MAP?
-
What is the normal range for ICP?
0 - 10 mmHg
-
What is the goal of CPP?
> 60 mmHg
-
What is the formula to calculate CPP?
-
Describe the presentation of increased ICP
- Change in LOC
- Change in pupil size & reaction
- Abnormal motor responses
- Decorticate
- Decerebrate
-
Describe Decorticate posturing
Adduction of upper extremities towards the "Core"
-
What is the significance of decorticate posturing?
Indicates damage above the cerebellum & brainstem (supra-tentorial)
-
Describe decerebrate posturing
Extension & hyperpronation of upper extremities
-
What does decerebrate posturing indicate?
Damage to brainstem or compression of the thalamus & brainstem
-
Identify the 3 components of Cushing's Triad
- HTN
- Bradycardia
- Respiratory changes
-
Describe the treatment of the Increased ICP patient
- Position patient
- Eyes forward
- 15-30 degrees reverse trendelenburg
- Limit noxious stimuli
- Suctioning/Invasive procedures
- Noise
- Atmospheric pressure changes
- Maintain euvolemia, normothermia & normal electrolytes
- Pharmacology:
- Sedation - benzos, propofol
- Analgesia - fentanyl
- NMBAsSystematic Approach to Herniation
-
Describe the Systematic Approach to Herniation
- Paralyze, ETI & slightly hyperventilate to a PaCO2 of ~ 32-35 mmHg
- If using ETCO2 don’t forget gradient correction
- What happens w/hypoventilation?
- “Cerebral Steal or Luxury Perfusion”
- What happens w/hyperventilation?
- "Reverse Steal or Robin Hood Effect”
- Assure adequate O2 delivery
- 100% for duration of transport
- Assure adequate fluid resuscitation 1st,
then consider - Mannitol
- Hypertonic saline
- ⇩ O2 demand by induction of barbiturate coma
- thiopental (Pentothal®) TOO SHORT ACTING
- phenobarbital (Luminal®) DRUG OF CHOICE
-
Describe subdural hematomas
- Blood btn the Dura & Arachnoid membranes
- Usually venous in nature
- High morbidity/mortality
- 3 types
- Acute: Symptomatic w/in 24°
- Subacute: Symptomatic w/in 2-10 days
- Chronic: Symptomatic after 2 weeks
-
Describe subdural hematomas in the elderly
Larger subdurals w/slowly developing symptoms d/t cerebral atrophy
-
Describe subdural hematomas in younger pops
- Rapid onset of symptoms w/marked ⇧ ICP
- Peds subdurals typically occur
- < 18 mos
- Look for bulging fontanelle & retinal hemorrhages
-
Describe epidural hematomas
- Bleeding btn the skull & the dura mater
- Usually arterial but can be venous
- Laceration of the middle meningeal artery in the temporal lobe area
-
Describe the presentation of epidural hematomas
- Classic symptomology – Transient loss of consciousness followed by a period of lucidity “Lucid Interval”
- Epidural bleeds cause uncal herniation
- Will result in dilation of the ipsilateral pupil w/contralateral neuro deficits/posturing
-
Describe subrachnoid hemorrhage
- Bleeding btn the arachnoid membrane & the
- pia mater
- Trauma is the most common cause
- Berri aneurysm 2nd most common cause w/rupture 2° HTN
-
Describe the presentation of subarachnoid hemorrhage
- “Worst Headache of My Life”
- N/V, stiff neck, visual disturbances, Δ LOC
- Confused w/meningitis
- No LP if Sub-A bleed possible
-
Describe intracerebral hemorrhage
- Hemorrhage in the brain parenchyma
- Produced from shearing & tensile forces
- Frequently occurs in the white matter of the frontal & temporal regions
- May be single or multiple & is associated w/contusions, subdural hematoma & diffuse axonal injury (DAI)
- Less common injury w/delayed onset of symptoms (24° or more after injury)
-
Describe intraventricular hemorrhage
- Bleeding into the ventricles as a result of severe brain trauma
- Result of shearing forces
- Greatly ⇧ mortality rate
- Usually found in frontal or temporal lobes
-
Describe mild concussion
- Rotational Force
- Reversible w/no persistent sequelae
- Retrograde amnesia of short duration
-
Describe Classic Concussion
- Rotational or direct force
- Reversible w/memory & info processing problems
- Brief LOC, retrograde & post traumatic amnesia
-
Describe Diffuse Axonal Injury [DAI]
- Diffuse shearing injury – rotational acceleration
- Irreversible w/profound neuro, psych & personality deficits
- Usually coma
-
Describe the 3 classifications of CVA
- Embolic – Most common
- Hemorrhagic – Bleeding into brain tissue
- Thrombotic – Least common
-
Describe the treatment of CVA
- Prevent additional insult
- Maximize Cerebral blood flow
- Control ⇧ ICP
- Manage associated conditions
- Thrombolytic therapy w/i 3 hrs of neurologic deterioration onset
-
Describe a linear skull fx
A line that extends toward the base of the skull
-
Describe a linear stellate skull fx
Multiple Fx that radiate from the compressed area
-
Describe a diastatic skull fx
Involves a separation of the bones at a suture line or a marked separation of bone fragments
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Describe a depressed skull fx
May be open or closed
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Describe a basilar skull fx
Fx of the base of the skull
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Describe the signs of a basilar skull fx
- Battle’s sign: Bruising behind the ear on the mastoid bone
- Periorbital Ecchymosis (Raccoon Eyes): Ecchymosis around the eyes
- Otorrhea: Bleeding from ear w/CSF leak
- Rhinorrhea: Bleeding from the nose w/a CSF leak
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What are the complications from skull fx?
- Intracranial Infections
- Hematomas
- Meningeal & brain tissue damage
- PneumocephalusAssociated nerve damage & palsies
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Differentiate btn the LeFort Fx Classifications
- LeFort I: Fx of the mandible
- LeFort II: Nose & maxilla separate from skull
- LeFort III: Through the zygomas; The face from the eyes down is free floating
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Define neurogenic shock
- Areflexia w/flaccid paralysis immediately or shortly after injury
- Parasympathetic dominance below the lesion
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Describe the classic presentation of neurogenic shock
- Hypotension
- Warm red skin below injury
- Absence of tachycardia
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Management of CHI is typically referred to as Triple-H Therapy. This consists of:
- HTN
- Hypervolemia
- Hemodilution
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Patients MOST likely to demonstrate an acute subdural include:
Pediatric patients
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Describe maternal physiological Δs
- HR ⇧ 15-20 bpm
- BP ⇩ in 2nd Trimester 5-15 torr & ⇧ in 3rd trimester 10 torr
- Cardiac Output ⇧ ~ 2 L/min
- Plasma volume ⇧ 40% ⇨ ⇧ clotting factors
- Placenta very high in tissue thromboplastin content
- RBC’s ⇧ but not @ same rate as plasma ⇨ dilutional anemia
- ⇧ volume ⇨ capillary engorgement ⇨ airway swelling
- Mallampati ⇧ 2-3 classes
- Failed airways 1:2230 vs 1:280 when Pg
- Heart elevates anteriorly & ↺ to left
- WBC ⇧
- Progesterone relaxes everything (sphincters,
- vasculature, etc)
- ⇩ Functional Residual Capacity [FRC] by ~ 20%
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Define the obstetrical term 'Dilation'
Refers to the extent of cervical dilation as judged by palpation
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Define the obstetrical term 'Effacement'
Relates to the thickness of the cervix & is expressed as a %. The cervix is normally about 2 cm thick & thins during labor. When thinned to 1 cm would be said to be 50% effaced.
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Define the obstetrical term 'Lie'
Refers to the longitudinal orientation of the fetus in relation to the longitudinal orientation of the mother
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Define the obstetrical term 'Station'
Refers to the fetal head in relation to the mother’s pubic bone & is expressed as a + or a - number as measured in cm
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Define the obstetrical term 'Presentation'
What is attempting to emerge 1st? Cephalic, breech or shoulder? (Cephalic – Vertex, brow or face)
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What are baseline FHTs?
120-160/min
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Define the importance of 'variability' as it relates to FHTs
The single most important predictor of fetal well-being
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What causes Poor variability in FHTs?
- Fetal hypoxia
- Meds given to mom
- Smoking
- Extreme prematurity
- Fetal sleep
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What do accelerations indicate?
- Usually GOOD
- Usually associated w/fetal movement & CNS
- response to stimuli
- Hypoxic fetus w/metabolic acidosis cannot
- accelerate the heart
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What causes Early Decelerations & of what diagnostic value are they?
- OK sign
- Typical vagal response to squeezing of head caused by contractions
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What are Late Decelerations & of what diagnostic value are they?
- BAD
- Indicate uteroplacental insufficiency causing the fetus to experience a hypoxic bradycardia
- Commonly associated with:
- PIH
- DM
- Smoking
- Late Deliveries
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Describe Variable Decelerations in FHR monitoring
- Not good but correctable
- Common during contractions, typically V or W shaped
- Caused by cord compression
- Shouldering” is common
- Look for ‘cord’ problems
- Prolapse
- Short
- Entanglement
- Nuchal
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What causes sinusoidal FHR patterns?
- Typical of fetal hypovolemia OR anemia
- Accidental tap of the umbilical cord during amniocentesis
- Fetal maternal transfusion
- Placental abruption
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Define fetal bradycardia
FHR < 120 for 5-10 min
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Define fetal tachycardia
FHR > 160 for 10 min
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Describe factors affecting fetal distress
- Assure fetal oxygenation: Give mom High flow O2 by NRB
- Maternal hypotension
- Initiate 250-500 cc IVF bolus
- Correct supine hypotension
- “Tank her up”
- Hypertonic or tetanic contractions: D/C oxytocin infusion
- R/O cord prolapse
- Assess for placental abruption
- Δ positions
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Describe S/S of Imminent Delivery
- VB
- Contractions more frequent than q 10 min
- ⇧ intensity
- Urge to push
- Crowning
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What steps should you take when dealing w/Pre-Term labor?
- ☑ 4 signs of Imminent Delivery
- Obtain status of amniotic membranes
- Determine cervical status
- L Lateral Recumbent
- Assess for infection
- Prophylactic Abx for Group B Strep
- Tocolytics
- MgSO4-: Watch 4 toxicity
- Terbutaline
- Monitor FHT, movement
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How do we monitor for mag toxicity?
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Describe the treatment of mag toxicity
- CaCl 4 the acute OD
- Push fluids w/diuresis [Renal excretion is very good]
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Drug Card: terbutaline
- terbutaline
- (Brethine®, Breathaire®)
- 0.25 mg sq q 15
- Pre-Term Labor
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magnesium sulfate Drug Card
- magnesium sulfate
- (MgSO4-)
- 4-6 gm bolus / 15-30 min, 2 gm/hr maint
- Preeclampsia, Pre-Term Labor
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oxytocin Drug Card
- oxytocin
- (Pitocin®)
- 20-40 units/1000 cc @ 125 cc/hr
- Post-Partum hemorrhage
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hydralazine Drug Card
- hydralazine
- (Apresoline®)
- 2 mg IVP q 5 min to DBP 90-100 mmHg OR 5-10 mg q 20 min
- PIH, Preeclampsia
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What etiologies may account for PIH?
- ⇧ Volume - Autoregulation Mismatch
- Placental Toxins
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What does HELLP stand for?
A syndrome where pts experience a myriad of symptoms including Hemolysis, Elevated Liver enzymes & a Low Platelet count
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Describe the presentation of PIH
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What population most at risk for PIH?
- African-American FemalesPrima Gravida
- Multi Gravida
- Very young maternal
- Advanced maternal age
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Describe guidelines for treatment of PIH, Preeclampsia & HELLP
- Watch for late decels & ⇩ variability as well as fetal movement
- MgSO4 4-6 G bolus followed by 1-2 G/hr
- Steroids betamethasone (Celestone®) ASAP
- Consider labetalol (Trandate®) 20 mg SIVP
- Consider hydralazine (Apresoline®) 2 mg SIVP
- Give diazepam (Valium®) PRN 4 seizure activity w/MgSO4 (MgSO4 inhibits cerebral vasospasm primarily)
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Describe the causes of AAA in pregnancy
- Gravid uterus ⇧ clonic pressure on distal aorta & femoral arteries
- ⇧ circulating volume
- ⇧ aortic ejection pressures
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How may the parturient pt's AAA presentation be misleading?
- CP similar to AMI
- May actually be complicated by an AMI
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How do you maximize fetal viability in the pregnant trauma pt?
Aggressively treat mom like you treat other trauma pts
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What are the risk factors for placenta previa?
- Uterine scarring
- Multiparity w/short intervals
- Post D&C
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Describe the typical presentation of placenta previa
Painless Bright red vaginal bleeding
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Describe the typical presentation of placental abruptio
Ripping or tearing pain w/dark or no evident blood loss
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Describe the treats posed by placental abruptio
- Exsanguination
- Placental insufficiency
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What does bleeding in the uterus cause?
Blood is irritating to the uterus ∴ it will initiate contractions
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Describe the management of the placental abruptio pt
- High flow O2, VS, Fluids
- Assess for contractions, fetal movement, FHTs, hemorrhage
- Continually reassess fundal height
- Consider tocolytics & blood products
- Watch for signs of DIC
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What measurement is helpful in uterine rupture?
Serial fundal height measurements
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How do FHTs respond to nuchal cord?
Variable decelerations
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Describe management of nuchal cord
- Gently loosen & draw down over head
- Clamp & cut before shoulders deliver if it is too tight to remove
- Focus is relieving cord tension before next contraction
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Describe treatment of umbilical cord prolapse
- Elevate presenting part off the cord w/a hand in the vagina to prevent cord compression
- Trendelenburg or knee-chest position
- Tocolytics to reduce pressure on the cord during contractions
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Describe management of the breech presentation
- Fetus should not be touched until cord has spontaneously delivered
- Palpate the cord for FHR
- After shoulders have delivered, rotate baby’s trunk so that the back is anterior & apply gentle downward traction
- Apply suprapubic pressure to facilitate delivery of the head
- Mauriceau’s Maneuver
- Do not attempt to deliver a footling breech
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Describe management of meconium delivery
- Suction mouth, posterior pharynx & nose after delivery of head, but before delivery of
- shoulders
- If baby is vigorous continue w/supportive care
- If baby is not vigorous suction mouth & trachea
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Define "vigorous" as it pertains to the newborn
- Strong respiratory efforts
- Good muscle tone
- HR > 100 bpm
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Describe management of postpartum hemorrhage
- Vigorous fundal massage
- Rapid infusion of 20-40 units of oxytocin (Pitocin®)
- methylergonovine (Methergine®) 0.2 mg IM
- Assess blood loss
- Replace fluids, blood
- Bimanual uterine compression
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Describe the management of uterine inversion
- Manual replacement if the uterus has not yet contracted down & cervix has not constricted
- Tocolytics if the uterus has contracted to relax the uterus & allow replacement
- DO NOT REMOVE THE PLACENTA
- oxytocin use post replacement
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Describe management of Amniotic Fluid Embolism (AFE)
- High flow O2, ETI PRN
- PEEP may be required
- Fluid resuscitation
- Hemodynamic monitoring
- Blood product replacement as needed
- FFP, Platelets, Cryo
- Anticipate severe fetal distress if syndrome presents prepartum
- Prepare for emergent post-mortum c-section
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Describe management of DIC
- Airway management
- Stop ongoing major hemorrhage
- Volume replacement
- Minimize needle sticks
- Blood products (FFP, platelets)
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What airway issues are seen with DIC?
- ⇧ sensitivity to aminosteroids (VEC & ROC)
- Possible prolonged effects of SUX
- Difficult airway/Failed airway more common
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