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1
Q

Burn center criteria

A

Partial thickness > 10-20% TBSA
Full thickness >5% TBSA
Burns to hands/face/feet/genitalia/major joints
Electrical/chemical burns
Inhalation injury
Major comorbidity or trauma
Pediatric

75% meet criteria

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2
Q

CO poisoning

A

Sequelae: seizures, syncope, coma, MI, lactic acidosis, pulmonary edema, neuropsych deficits
RA: 300 min half life
100% NRB: 90 min
Hyperbaric: 30 min

Evaluation: CXR and SpO2 may be normal, obtain carboxyhemoglobin.
(0% = non-smoker, 10-20% in smoker, >30% = severe, consider hyperbarics, risk coma/death)

From combustion of carbon products

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3
Q

Hyperbaric indications

A

pH <7.1
Myocardial ischemia
Pregnancy
CoHb > 40%
Normal CoHb but pt is symptomatic

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4
Q

Cyanide toxicity

A

Inhibits cell from receiving and using O2 in mitochondria, forces mitochondria into anaerobic metabolism, interrupts cellular metabolism
Monitor serum lactate and EtCO2
Antidote: High dose Vitamin B12 Hydroxocobalamin

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5
Q

Parkland

A

4 mg x kg x % TBSA burned = amount crystalloid over 24 hr
1/2 in 1st 8
1/2 in remaining 16

Criticized for over-resuscitating

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6
Q

Modified Brooke

A

2 mg x kg x % TBSA burned = amount LR over 24 hr
1/2 in 1st 8
1/2 in remaining 16

Developed in army, optimized for young, healthy, physically fit

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7
Q

Quick Calculation

A

(Kg x TBSA) / 8 = hourly fluid

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8
Q

Rule of 10s

A

% TBSA (to nearest 10th) x 10 = initial hourly rate for adults 40-80 kg.
Increase rate by 100 mL/hr for every 10 kg above 80

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9
Q

Guidelines to resuscitation

A

HR, BP, lactate, CVP,
UO = 0.5 mL/kg/hr (30-50 mL/ hour for adult)

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10
Q

Over resuscitation

A

Compartment syndrome, ARDS, edema, infection, mortality

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11
Q

Superficial (epidermal)

A

Confined to epidermis, not included in calculation TBSA
Mild erythema without blisters, + cap refill, + pain
Heal spontaneously with cleansing and topical antibiotic cream

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12
Q

Partial thickness (dermal)

A

Destruction of 1/3 of dermis
Blistered, red, painful
Healing: 1-2 weeks
Tx: Debride large blisters, non-stick dressing

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13
Q

Partial thickness (deep dermal)

A

Most of dermal layer damaged
White/charred, difficult to distinguish from full thickness
4-10 week healing

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14
Q

Full thickness

A

3: Through epidermis and dermis, down to SubQ fat, fascia
4: Down to muscle or bone
Painless, leathery, waxy, charred or red but does not blanch
Will not heal well w/o grafting

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15
Q

Silver sulfadiazine

A

Good microbial, fungal and pseudomonal
coverage, some eschar penetration
For partial and full thickness wounds
Avoid in sulfa allergy, leukopenia, pregnancy

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16
Q

Medihoney

A

Antimicrobial, analgesic, provides and
draws out wound moistures
For superficial and full thickness
Low pH, may cause stinging

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17
Q

Bacitracin

A

Good gram negative and gram positive
coverage
For superficial and full thickness
Occasional heat rash from ointment

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18
Q

Mupirocin

A

Antimicrobial (gram positive only); used
for MRSA and VRE, wounds unresponsive to SSD or bacitracin

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19
Q

Gentamycin

A

Antimicrobial for infected wound unresponsive to traditional topicals

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20
Q

Chemical burns

A

Most from acids or alkali. Cause progressive damage/injury until chemicals inactivated

acid-coagulation necrosis limits penetration
alkali-combine with cutaneous lipids and dissolve into skin

Remove all clothing, irrigate w tepid water, should consider to be deep partial or full thickness

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21
Q

Electrical burns

A

what is visible on the skin is not fully indicative of level of injury
MOA: direct tissue injury + conversion to thermal burns + associated blunt trauma
CP: arrest/Vfib, MI or contusion
Musculoskeletal: muscle tetany can cause fx, compartment syndrome, rhabdo, necrosis or osteo from heat
Renal: hypovolemia, rhabdo
CNS: spinal fx, delayed myelitis

** Endpoint resuscitation for rhabdo = 100 cc/hr

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22
Q

Trauma lethal triad

A

Hypothermia
Coagulopathy
Acidosis

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23
Q

Primary hypothermia

A

Result of a direct exposure to cold in
previously heathy individual

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24
Q

Secondary hypothermia

A

Occurs in ill person with medical
conditions
Decreased heat production
Impaired thermoregulation
*Can occur in warm environment

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25
Q

Mild hypothermia

A

32-35
Subtle shivering, lethargy
Critical coagulopathy below 34

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26
Q

Moderate hypothermia

A

28-32
Decreased LOC, cardiac disturbances, pupil dilation
decreased RR

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27
Q

Severe hypothermia

A

20-28
Complete CV and nervous system collapse (absent motor and reflex functions)
Cardiac standstill @ 20

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28
Q

Profound hypothermia

A

14-20
Cardiac standstill @ 20

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29
Q

Deep hypothermia

A

<14

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30
Q

Radiation

A

Occurs when heat passes from a warmer to cooler area through the air without direct contact
55-60% heat loss

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31
Q

Conduction

A

Transfer of heat through direct contact with cool objects
15% heat loss

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32
Q

Convection

A

Movement of air or liquids over the skin

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33
Q

Evaporation

A

Transfer of heat through moist skin/mucous membranes/wounds
30% heat loss

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34
Q

Cold diuresis

A

Fluid shifts from vascular to interstitial space, decreased ADH, decreased Na/H2O absorption
*Can’t use UO as measure of EOP

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35
Q

Passive external rewarming

A

Hemodynamically stable, standard of care to increase temp 0.5-2 degrees/hr and prevent further heat loss
Warm blankets, remove wet clothes

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36
Q

Active external rewarming

A

Faster rewarming @ 1-2.5/hr
Convective air blankets/warm water immersion/radiant heat

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37
Q

Afterdrop

A

S/p direct rewarming, peripheral vasodilation results in transport of cooler peripheral blood to core, causing decreased temp

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38
Q

Rewarming shock

A

Decreased BP associated with vasodilation and volume depletion (cold diuresis)`

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39
Q

Active core rewarming

A

Severe hypothermia, rapid rewarming of vital organs by providing heat over large surface areas
Peritoneal lavage (1-2.5 C/hr)
Closed thoracic chest lavage
Airway rewarming (humidified O2)

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40
Q

Extracorporeal rewarming

A

Gold standard for severely hypothermic pt
Hemodialysis: for moderate rewarming in pt w/o HD instability. contraindicated in trauma d/t need for heparinization. increase temp 2-3 d/hr
Arteriovenous rewarming (specifically developed for trauma patients BUT dependent on maintaining adequate BP) SBP must be >80
Venovenous rewarming (ECMO): less invasive, not dependent on BP
Cardiopulmonary bypass *Gold standard for severe hypothermic trauma pt in cardiac arrest-oxygenate and perfuse organs + rewarm pt despire Vfib or asystole (contraindicated in trauma)

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41
Q

Rescue collapse

A

Cardiac arrest associate with
extrication and transport of a patient
with severe hypothermia

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42
Q

Bariatric surgery indications

A

BMI > 40 or BMI > 35 + comorbidity

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43
Q

Malabsorptive/restrictive

A

Roux en Y gastric bypass
Bypass stomach and part of intestines. More complicated procedure Cannot be revised to gastric sleeve
Major complication = dumping syndrome
70% weight loss over 2 years, superior for management of DM

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44
Q

Restrictive

A

Gastric sleeve
Simpler procedure, can be revised to gastric bypass if needed
60% weight loss over 2 years
Common complication = strictures

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45
Q

Dumping syndrome

A

N/V, tachycardia, abdominal cramping, diarrhea after high sugar meals (esp common after Roux en Y)

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46
Q

Bariatric surgery complications (early)

A

PE
Gastrointestinal leak
Infection

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47
Q

Cirrhosis

A

LFT derangements: Albumin, INR, Plt
Top causes: viral hepatitis, fatty liver, EtOH, hemochromatosis
Dx: Biopsy = gold standard
Decompensated: ascites, portal HTN, hepatic encephalopathy, hepatorenal syndrome, liver CA
Tx: prophylaxis and prevent progression

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48
Q

Albumin

A

3.5-5.5
Colloid oncotic pressure, synthesized by the liver
Complications if low: 3rd spacing, ascites, edema, anascara

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49
Q

INR

A

Normal = 1
Vitamin K Dependent clotting factors (II, VII, IX, X) synth by liver
Complications if derangement: bleeding, bruising, prolonged PT

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50
Q

Plt

A

Low for 2 reasons in liver failure
1. TPO synthesized by liver
2. Splenomegaly d/t portal HTN = increased sequestration
Derangements = bleeding, bruising

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51
Q

AST

A

< 40
Not totally specific for liver, also found in heart, skeletal muscle, kidneys, brain
Can indicate hepatic or non-hepatic injury
Elevated in alcoholism, steatohepatitis

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52
Q

ALT

A

< 40
More specific for liver
Elevations indicate liver injury, steatohepatitis

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53
Q

Alkaline phosphate

A

<100
Found in biliary tree, bone, placenta
Elevated when obstruction in biliary tree

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54
Q

Bilirubin

A

Total <1
Released during RBC breakdown, travels to liver where indirect is conjugated into direct, then excreted in stool
Elevated indirect: hemolysis, liver failure, conjugation defect
Elevated direct: Cholestasis, obstruction

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55
Q

Cholelithiasis

A

Gallstones, no issues

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56
Q

Biliary colic

A

gallbladder contracts and pushes
stones back and forth into the cystic duct, pain <6 hours associated with N/V (no fevers or chills)

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57
Q

Cholecystitis

A

biliary colic that does not resolve > 6
hours, causing inflammation, N/V/RUQ pain + fever

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58
Q

Choledocholithiasis

A

Gallstones in the common bile duct

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59
Q

Cholangitis

A

Gallstones in the CBD causing infection/fever and/or obstruction

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60
Q

Charcot’s triad

A

Cholangitis: RUQ pain, fever, juandice

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61
Q

Raynaud’s pentad

A

Cholangitis:
Charcot’s triad (RUQ pain, fever, jaundice)
+
Hypotension
+
AMS
=
Very very sick, sepsis

62
Q

Hepatocellular injury

A

AST/ALT > 40

+/- Indirect bili > 1

(out of proportion to elevations to Alk phos or D bili)

63
Q

Cholestatic injury

A

Alk phos > 100
Direct bili > 1

+/- AST/ALT > 40

(Alk phos and D bili elevated out of proportion to AST/ALT)

64
Q

HAV

A

RNA
Transmission: Fecal-oral
Vaccine: Yes
Cirrhosis risk: No
Tx: supportive

65
Q

HBV

A

DNA
Transmission: Blood, body fluid, perinatal
Vaccine: Yes
Cirrhosis risk: Yes
Tx: Antivirals, supportive, close monitoring

66
Q

HCV

A

RNA
Transmission: Blood, body fluid, perinatal
Vaccine: No
Cirrhosis risk: Yes
Tx: Antivirals

67
Q

HDV

A

RNA
Transmission: Blood, *needs HBV to enter liver cell
Vaccine: Yes (HBV)
Cirrhosis risk: Yes
Tx: Antivirals, supportive, close monitoringR

68
Q

HEV

A

RNA
Transmission: Fecal-oral
Vaccine: No
Cirrhosis risk: No
Tx: Supportive, pregnant people may develop liver failure

69
Q

Ammonia

A

From protein metabolism by gut bacteria, cleared by the liver.
If not adequately cleared, accumulates and easily crosses BBB causing hepatic encephalopathy

70
Q

AKI

A

Loss of GFR over hours to days, inability to excrete daily solute

71
Q

Pre-renal azotemia

A

When blood flow to kidneys is decreased, filtration lost before perfusion
Kidney autoregulates blood flow
–Afferent (blood in): vasodilatory prostaglandins (can be inhibited by NSAIDs)
–Efferent (blood out): Backpressure mediated by angiotensin ii (inhibited by ACEI/ARBs)

Causes: volume depletion from over-diuresis, N/V/D, hemorrhage, 3rd spacing, CHF, hypotension, B/L renal artery stenosis/occlusion

Dx: Blood BUN > Cr (more than 10:1)
Urine: Normal UA with high SpGr and urine osmolality. Retention of sodium = low urine Na (<10) and low fractional excretion of sodium (<1%)

Tx: Stop ACE-I/ARB, NSAID, correct hypotension, give fluids, avoid nephrotoxins

72
Q

Obstructive uropathy (post-renal)

A

Causes: kinked foley, BPH, malignancy, anti-cholinergics, ureteral obstruction
Dx: bland UA, renal US
Tx: insert/flush foley, BPH meds, D/C anticholinergics

73
Q

Acute tubular necrosis

A

Blood flow to kidneys is poor, perfusion lost and kidney cells die, causing decreased function
Tubules not working, SO: Can’t concentrate urine, can’t conserve Na, can’t excrete K
About 3 weeks to recovery
Causes: Severe volume depletion, sepsis, shock, toxins
Dx
Urine-high urine sodium, fractional excretion of sodium > 1, + muddy brown granular casts and renal tubular epithelial cells
Does not immediately reverse w fluid administration

Complications: volume overload, metabolic acidosis, electrolyte disturbances, toxin build up (uremia)
Some patients will require dialysis

74
Q

Allergic interstitial nephritis

A

Allergy/inflammation to the kidney –> loss of function
Common meds: PCN, Cephalosporins, NSAIDs, PPI
Dx: WBC on UA (negative Urine Cx) eosinophils in blood/urine, +/- fever w/o other cause, unexplained rash, renal biopsy
Tx: Stop offending med, steroids to preserve renal function long term, may req dialysis

75
Q

Acute glomerulonephritis

A

Autoimmune reaction in the kidney
Dx: RBC and RBC casts in urine, proteinuria, HTN, renal biopsy
Tx: immunosuppression, dialysis maybe necessary

76
Q

Tetraplegia

A

Injury to cervical spinal cord causing loss of muscle strength in 4 extremities C1-T1

77
Q

Paraplegia

A

injury to the thoracic spine (T2-T12)

78
Q

ASIA A

A

Complete: No sensory/motor function, including sacral segments

79
Q

ASIA B

A

Sensory recovery: Sensory but no motor below level of injury, sacral sparing

80
Q

ASIA C

A

Motor recovery/non-functional: Motor function preserved below injury, but most key muscles unable to resist gravity (less than 3/5 strength)

81
Q

ASIA D

A

Motor recovery/functional: Motor preserved below injury, most key muscles greater than 3/5 strength

82
Q

ASIA E

A

Complete recovery

83
Q

Posterior cord syndrome

A

Very rare, most often occurs with tumor invading cord (less often traumatic)
Loss of proprioception, ataxia. Maintain pain, temp, motor function

84
Q

Central cord syndrome

A

Often seen in older adults in combo w/ stenosis and hyperextension
B/L loss of motor/sensory in upper extremities (more weakness distally).
Preservation of function in
lower extremities

85
Q

Anterior cord syndrome

A

Damage to anterior 2/3 from disk, tumor, herniation
Loss of motor/pain/temperature below the level of injury. Preserved proprioception
(spares dorsal column)

86
Q

Brown-Sequard Syndrome

A

Very rare. Hemisection lesion of cord. Good prognosis
Ipsilateral loss of motor and proprioception
Contralateral loss pain/temp

87
Q

Cauda equina

A

lumbarsacral nerve roots, affects bowel/bladder. Often caused by
lumbar disk herniation

88
Q

Spinal cord concussion

A

transient neurologic deficit without any apparent structural damage
Common in young athletes, typically resolves within 48 hours

89
Q

Neurogenic shock

A

Hemodynamic instability in the setting of SCI
Vasodilation (hypotension) + vagal stimulation (bradycardia) = warm shock
+/- hypothermia
Most at risk within 1st week after injury, most common in T6 or higher.
Treatment: Fluids first, then NE (vasoconstricts, positive inotrope) or DA
Atropine as needed for bradycardia

90
Q

Autonomic dysreflexia

A

Triggered by noxious stimuli below
the level of injury -> leads to overstimulation of the autonomic nervous system
Sx: Hypertension, headaches, anxiety, diaphoresis, nausea
Hypertension can be life-threatening: MI, stroke, pulm edema
Tx: sit patient up, remove tight clothing and remove noxious stimuli. May require antihypertensive (nifedipine,
captopril), can lead to medical emergency
*Can occur at any time in life after SCI

91
Q

GERD

A

Lower esophageal sphincter (involuntary smooth muscle) doesn’t close properly, leading to ascending of gastric acid causing chest pain and acidic taste, regurgitation of
food, and burning of the larynx (cough)
Sx: CP/heartburn, regurgitation, acidic taste in mouth, mild dysphagia, unexplained cough

92
Q

H2 blockers (ranitidine, famotidine)

A

Can be taken on PRN basis (not recommended for GERD with complications) blocks initial part of acid secretion pathway

93
Q

PPI (Omeprazole, Lansoprazole)

A

Blocks the final part of the acid secretion pathway (more effective)
* Take 30 minutes before first meal (H-K ATPase most active after prolonged fast)
* Take for 8 weeks

ADE: PNA, C. diff, Hip fx, Kidney disease, interactions with other meds

94
Q

Barrett’s esophagus

A

Columnar metaplasia: Usually there are squamous cells in the lower portion of the esophagus. If GERD causes frequent acid exposure, the cells change into columnar cells that can withstand the acidity –> dysplastic cells can be precancerous

Nondysplastic (+metaplasia): surveillance EGD 3-5 years

Low grade dysplasia (precancerous): Radiofrequency ablation

High grade dysplasia: endoscopic eradication therapy

Start PPI therapy

95
Q

H pylori

A

Gram negative bacteria that produces urease. Urease takes urea in the stomach and
hydrolyzes it into ammonia. Ammonia acts as a cloud to buffer H.pylori from gastric acid. Spiral shape, flagella, and acid buffer allow
it to penetrate through the gastric mucus
layer and into the underlying tissue

If untreated: risk maltoma

Tx: High dose BID PPI

And EITHER
Amoxacillin + Clarithromycin

Or
Metronidazole, Tetracycline, Bismuth subsalicylate

96
Q

Acute pancreatitis

A

Acute inflammation of the pancreas as
defined by two of the following three:
* Acute epigastric pain often radiating to the back
* Elevation of lipase or amylase > 3x upper limit of normal
* Pancreatic fat stranding or enlargement on CT/MRI

+need RUQ US to r/o gallstones

Common causes: alcohol, gallstones, certain meds, post ERCP, high TGs
Complications: fluid collection, pseudocyst formation, necrosis, shock/ARDS

Tx: supportive fluids, pain control, bowel rest, EtoH cessation/tx for TGs

97
Q

Crohn’s

A

IBD
Anywhere (mouth to anus) but uniquely the terminal ileum and perianal area
Transmural (whole wall thickened)/ cobblestoning
Inflamed areas can lead to strictures and then small bowel obstructions
Fistulas
All need surveillance colonoscopy

98
Q

Ulcerative colitis

A

IBD
From rectum up the colon to the splenic flexure (no small bowel), contiguous lesions
Superficial ulceration (area closest to lumen affected)
Only do surveillance colonoscopies if disease
beyond rectum

99
Q

Thrombocytopenia

A

< 150 k/uL
Clinical manifestations: mucocutaneous bleeding, petechiae, purpura, epistaxis, gingival bleeding, GI, menorrhagia
ICH (rare unless severe)

Most major bleeding occurs < 50k/uL
Immediate hospitalization: 10-20 k/uL

100
Q

Pseudothrombocytopenia

A

Laboratory artifact, usually due to EDTA-dependent antibodies
Solution: repeat CBC in a heparinized or sodium citrated tube

101
Q

ITP

A

Dx of exclusion
B cells make auto antibodies (ant-plt), tag plt for destruction –> destroyed by macrophages.
Common in peds after viral infection, unclear etiology in adults
Tx:
Reduce antibody production: corticosteroids, Rituximab
Reduce antibody mediated clearance: Corticosteroids, IVIG, Anti-Rh, splenectomy
Enhance plt production: TPO

102
Q

Drug induced thrombocytopenia

A

Usually 1-2 weeks after initiating drugs
Long list of offending meds: includes quinine, many Abx, Gp IIb/IIIa antag
Tx: cessation of drug

103
Q

HIT

A

PF4 (from plt release) forms complex w heparin. Some patients make an auto-Ab to this complex, those complexes can activate other platelets–> thromboembolic and plt consumption
Low plt count BUT not bleeding, tendency towards thrombosis
5-14 days after initiation of heparin
Tx: Cessation, initiation of non-Hep anticoag, lifelong avoidance of heparin
**Unfractionated more likely than LMWH

104
Q

TTP

A

Extremely rare
ADAMTS13 normally cuts VWF. Insufficient ADAMTS13, large VWF molecules bind to plt, clump and get stuck
Lab: Decreased plt and RBC, + schistocytes (from RBC destruction)
Sx: seizures, stroke, confusion, arrhythmia, MI, renal failure, abd pain –> 90% mortality
Tx: Plasma exchange aphersis: Give ADAMTS13 AND inhibit Ab to ADAMTS13, aphersis removes Ab and ULVWF, and FFP is transfused back

105
Q

DIC

A

Activation of clotting factors/plt –> consumption
Clotting and bleeding
Common etiology: sepsis, CA, trauma, obstetrical emergency
Lab findings: decreased fibrinogen, elevated D-dimer, prolonged Pt/PTT, thrombocytopenia
Tx: Underlying cause, give blood products if bleeding

106
Q

Calcineurin inhibitors (Cyclosporine, Tacrolimus)

A

Immunosuppressive agents: Inhibit activation of T cell lymphocytes
Levels must be monitored closely, drugs given exactly as scheduled without missed doses
Interactions: any drugs that inhibit/induce CYP3A4 or P450
—Antifungals, CCBs, Macrolides, Grapefruit juice will increase level
—AEDs, Anti-TB Abx, St. John’s Wort will decrease level
ADE: Nephrotixicity, HTN/HLD, hyperglycemia, neurotoxicity

107
Q

Antiproliferative agents (CellCept, Myfortic)

A

Immunosuppressive agents: Prevent B and T cell proliferation
ADE: Myelosuppression (anemia), GI intolerance, pancreatitis

108
Q

mTOR Inhibitors (Sirolimus, Everolimus)

A

Immunosuppressive agents: Inhibit T cell lymphocyte proliferation
ADE: Poor wound healing, hyperTG, myelosuppression, proteinuria, LE edema, GI ulceration
*Not as commonly used (esp. immediately post-op) d/t wound healing

109
Q

Corticosteroids

A

Immunosuppressive agent: Affect function of leukocytes
Used for induction, maintenance, rejection –> start @ high doses and wean down as able
ADE: hyperglycemia, HTN/HLD, osteoporosis, mood swings, weight gain, acne, gastric ulcers, poor wound healing, cataracts, myopathy

110
Q

Infection prophylaxis (Txp)

A

6-12 months post-op txp when immunosuppression @ highest levels
Fungal–Nyastin/Mycelex for thrush prevention
Bacterial–Bactrim for PCP/toxoplasmosis
Viral–Valganciclovir for those w/ increased risk ZMV, otherwise Valacyclovir for HSV/VZV prophylaxis

111
Q

Txp adjunctive meds

A

Anti-HTN
Statins
BG management
GI prophylaxis
ASA
Pain management
Supplements: Vitamins, Ca, Mag, Iron

112
Q

Hyperacute rejection

A

Blood or antibody incompatibility

113
Q

Acute cellular rejection

A

T cells infiltrate tissue of transplanted organ
Tx depends on timing and severity
Baseline immunosuppression augmented
Moderate treated w steroids
Severe treated w monoclonal or polyclonal antibody preparations which deplete lymphocytes involved in rejection

114
Q

Chronic rejection

A

Immune mediated vessel injury. Months-years after txp. Intimal hyperplasia of graft blood vessels which interrupts circulation and eventually causes decline in graft function
Greatest challenge in long term survival

115
Q

Antibody mediated rejection

A

Antibodies form against donor tissue antigen
D/t inadequate immunosuppression
Can lead to severe graft dysfunction
Tx: plasmapheresis, IVIG, Rituximab

116
Q

Kernig’s sign

A

Severe stiffness of the hamstrings causes an
inability to straighten the leg when the hip is flexed to 90 degrees.

117
Q

Brudzinski’s sign

A

Severe neck stiffness causes a patient’s knees
and hips to flex spontaneously when neck is
flexed

118
Q

Acute bacterial meningitis

A

Fever, nuchal rigidity, AMS (+HA/photophobia)
Infection arises from nasopharynx, bloodstream, penetration of BBB
LP for every pt unless specifically contraindicated (CT 1st to R/o lesion or increased ICP)
Dx: CSF WBC > 1000 w/ > 80% neutrophils
Protein 100-500 (high)
Glucose < 40 (very low)
Common causes: strep pneumo, Neisseria meningitis/H flu (young), Listeria monocytogenes (old/immunocompromised)
Tx: Dexmethasone + 3rd Gen Ceph AND Vanc (+ampicillin for old/immunocompromised)
Tx: analgesia, antipyretics, IV isotonic hydration, anticonvulsants

119
Q

Encephalitis

A

AMS, motor/sensory deficit, speech/movement disorders, personality changes

120
Q

Meningococcal septicemia

A

Meningococcal meningitis when it becomes systemic
Loss of limb
Organ damage
DIC
Death

121
Q

Tuberculous meningitis

A

Occurs years after primary infection
Most commonly affects meninges, may invade cerebral/spinal tissue
Can progress from non-specific symptoms to death over three weeks if untreated
Dx: AFB in CSF smear
Tx: Isoniazid, Rifampicin, Pyrazanimide

122
Q

Cerebral abscess

A

Primary infection that spreads to brain
1) initial: HA, chills, fever, malaise, confusion, drowsiness, speech disorder
2) expansion: similar presentation to tumor, HA w increasing severity, confusion, drowsy
-> stupor
Unstable VS if increased ICP
WBC/Blood Cx usually normal, LP typically not recommended d/t increased ICP
Screening: HCT, MRI
Tx: Surgical drain or excision, correction of primary source, long term Abx

123
Q

Spinal epidural abscess

A

Often associated with vertebral osteomyelitis (thoracic most common)
Presentation: back pain tender to percussion, pain r/t leg, bowel/bladder dysfunction, weakness, fever, encephalopathy, meningismus w Kernig’s sign
Staph aureus most common (3rd gen ceph, vanco)
Dx: CBC, ESR, LP, Blood Cx, MRI
Tx: Surgery or IR guided biopsy

124
Q

Viral meningitis

A

Usually enters host passively via skin or mucosa (resp, GI, GU)
CSF Cell count: lymphocytes/monocytes elevated with normal glucose and protein, PCR detection
Tx: Supportive

125
Q

Acute viral encephalitis

A

Viral infection of the brain and meninges with an associated inflammatory response of the CSF
Rapid symptom onset
May see following childhood infections
Tx: Rapid initiation of acyclovir 10 mg/kg three times daily intravenously due to the high mortality associated with HSV encephalitis when treatment is delayed

126
Q

HSV encephalitis

A

Hemorrhagic viral encephalitis localizing to
the temporal lobes
Presentation: confusion, disorientation progressing to coma w/in days, complex partial seizures, olfactory hallucinations, hemiparesis
Dx: MRI and CSF
Tx: start immediately on acyclovir (PCR may be negative for 1st 48 hours)

127
Q

Neurosyphilis

A

Spirochetzal infection caused by Treponema pallidum
1st event = sore on the skin
CNS involvement in 7% untreated cases
Progressive dementia with memory impairment, Argyll Robertson pupils
Tx: PCN

128
Q

Argyll Robertson pupils

A

Pupils constrict with accomodation but not when exposed to bright light

129
Q

Toxoplasmosis

A

Parasitic infection
Acquired from: perinatal, unwashed veg/undercooked meat, cat droppings
Tx: Sulphadiazine and pyrimethamine
with folic acid for 6 weeks

130
Q

Prion disease

A

Neurodegenerative diseases with long
incubation periods and rapid progression
once clinical symptoms appear
–neuronal loss
–proliferation of glial cells
–absence of an inflammatory response
–the presence of small vacuoles within the
neuropil producing a spongiform
appearance

131
Q

C-spine

A

Smaller bones require ligaments to hold together. Can have unstable/mobile spine in the absence of fractures/bone trauma

132
Q

Primary injury (SCI)

A

mechanical disruption, transection, distraction of spinal cord (ie fractures, penetrating injury, hematoma or abscess, metastatic disease)
Goal is to prevent progression

133
Q

Secondary injury (SCI)

A

hypoperfusion or anoxia (ie vascular injuries, thrombosis, shock)
Dynamic process
Necrotic cell death/pro-apoptotic signaling, inflammatory cytokines–> scarring –> no ability for regeneration of axons where scar tissue has formed

134
Q

Sacral sparing

A

Some signal still innervates sacral nerves (bowel/bladder). Does pt have rectal tone? IF yes, incomplete/better prognosis.
ASIA B-E

135
Q

Intubate? (SCI)

A

C3-5 = diaphragm
T1-10 = Intercostals
T10-12 = Abdominal muscles

Absent cough @ C1-2
FVC 20% norm @ C3-6
FVC 30-50% norm @ T2-T4

Airway protection is key

136
Q

MAP Goal SCI

A

85-90 for 7 days
Adequate resuscitation needed to maintain cord perfusion. Cervical/high thoracic injuries can cause vasoplegia d/t decreased sympathetic tone

137
Q

VTE Prophylaxis (SCI)

A

LMWH initiated w/in 72 hours (pending ESS approval) – 3 months/rehab phase

138
Q

Transplant Complications

A

Rejection

Heart Failure
–#1 COD in kidney txp, major cause M&M in all solid organ txp
–Increased risk d/t HTN/HLD, DM, immunosuppression ADE, chronic rejection
–Modify risk factors

HTN
–Keep BPs <130/80, take at home measurements

DM
–ADE of tacrolimus/CNIs and corticosteroids

CKD
–Pt may have chronic renal insufficiency prior to txp + nephrotoxicity from CNIs
–Early referral to renal

Osteoporosis
–Majority of bone loss 6-12 mo. post-op when corticosteroids are highest
–DEXA screening prior to surgery
–Vit D, Ca, bisphosphonates

HLD
–Preexisting or ADE from immunosuppression
–Caution w/ statins: interactions w/ CNIs can cause increased level (CYP enzyme competition) and increase risk of rhabdo

Malignancy
–Squamous cell skin cancer in older, fair skinned pt
–Post-transplant lymphoproliferative disorder w/ immunosuppression (esp after EBV and CMV primary infections)
–Can occur from transmission from donor

Infection
–CMV: At highest risk if pt or donor had Hx CMV

139
Q

Kidney txp

A

Common causes: HTN, DM, polycystic kidney disease, lupus
**For T1DM: often kidney/pancreas txp

UTIs common after txp
Elevated Cr can be d/t UTI, dehydration, or rejection. Give fluids, infectious workup, cons renal and txp service

AlloSure is blood test for kidney rejection

40-60% survival @ 10 y (depending on living vs deceased donor)

140
Q

Liver txp

A

Common causes: HCV, hepatocellular carcinoma, NASH

Usually only on tac 8-12 months post txp
Monitor for recurrent disease (esp if txp needed because of NASH or autoimmune)

Rejection presentation: fever, pain at txp site, jaundice

50% survival at 10 y

141
Q

Heart txp

A

Common causes: ischemic/dilated cardiomyopathy, congenital heart disease

Rejection typically mimics HR

D/t denervation of heart post-txp, pt relies on catecholamines to increase HR w/ activity
–fast activities very difficult for pt
–atropine ineffective in codes

Avg resting HR ~90 (110-120 tachycardia common)

50-60% survival at 10 y

142
Q

Lung txp

A

Common causes: COPD, CF, PPH, ILD

Rejection suspected w/ decreased spirometry readings, SOB, CXR w effusions (often mimics infection)
Dysphagia common, high risk for aspiration PNA
Transplanted organ in constant contact w environment = increased infection risk

25% survival @ 10 y

143
Q

Hypothermia complications

A

Rescue collapse
Pulmonary edema and acute resp failure after rewarming
Multiorgan failure

Consider targeted temperature management 24 hr

144
Q

Endpoints to resuscitation (hypothermia)

A

Hyperkalemia >10
pH < 6.5
Severe coagulopathy
Persistent asystole despite temp >32

145
Q

Metabolic response hypothermia

A

Early increased metabolic rate/shivering
Late: decreased metabolic rate (1c decrease = 10% met. decrease)
Respiratory and metabolic acidosis
Anaerobic metabolism = production of lactate
Hyperkalemia

146
Q

CV response hypothermia

A

Increased PR, QRS, QT intervals
Osborn wave (J wave)
ST depression
T wave inversion

Vasoconstriction, decreased CO/contractility
Bradycardia

Dysrhythmias:
Vfib at 28C
Asystole at 25 C

147
Q

Pulm response hypothermia

A

Decreased RR
Decreased cough
Decreased mucociliary action/increased secretion
Shift to L in oxyhemoglobin dissociation curve

1C decrease = O2 consumption decrease by 5-15%

148
Q

Neuro response hypothermia

A

Decreased LOC progressing to coma
Cerebral autoregulation
Cerebral blood flow (6%/1°C), decreased cerebral metabolic demand
Pupil dilation (28-32 °C)
Absent motor and reflex functions @ <27 °C

149
Q

GI response hypothermia

A

Decreased motility/liver function/insulin release from pancreas
Ileus
Bacterial translocation
Stress ulceration

150
Q

Heme response hypothermia

A

Plt dysfunction
Enhanced fibrinolysis
Alterations in enzyme function
Increased blood viscosity
Hemoconcentration

Critical coagulopathy @34

151
Q

AST/ALT >1000

A

Tylenol toxicity
Viral hepatitis
SHOCK liver
HELLP
Budd-Chiari
Autoimmune

152
Q

SHOCK liver

A

Hypoperfusion liver injury

Sepsis
Hypovolemia/Hemorrhage
Obstruction
Cardiogenic
Kombos of the above

1 cause of AST/ALT > 1000

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