1 Flashcards
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
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
3
Q
Hyperbaric indications
A
pH <7.1
Myocardial ischemia
Pregnancy
CoHb > 40%
Normal CoHb but pt is symptomatic
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
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
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
7
Q
Quick Calculation
A
(Kg x TBSA) / 8 = hourly fluid
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
9
Q
Guidelines to resuscitation
A
HR, BP, lactate, CVP,
UO = 0.5 mL/kg/hr (30-50 mL/ hour for adult)
10
Q
Over resuscitation
A
Compartment syndrome, ARDS, edema, infection, mortality
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
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
13
Q
Partial thickness (deep dermal)
A
Most of dermal layer damaged
White/charred, difficult to distinguish from full thickness
4-10 week healing
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
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
16
Q
Medihoney
A
Antimicrobial, analgesic, provides and
draws out wound moistures
For superficial and full thickness
Low pH, may cause stinging
17
Q
Bacitracin
A
Good gram negative and gram positive
coverage
For superficial and full thickness
Occasional heat rash from ointment
18
Q
Mupirocin
A
Antimicrobial (gram positive only); used
for MRSA and VRE, wounds unresponsive to SSD or bacitracin
19
Q
Gentamycin
A
Antimicrobial for infected wound unresponsive to traditional topicals
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
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
22
Q
Trauma lethal triad
A
Hypothermia
Coagulopathy
Acidosis
23
Q
Primary hypothermia
A
Result of a direct exposure to cold in
previously heathy individual
24
Q
Secondary hypothermia
A
Occurs in ill person with medical
conditions
Decreased heat production
Impaired thermoregulation
*Can occur in warm environment
25
Mild hypothermia
32-35
Subtle shivering, lethargy
Critical coagulopathy below 34
26
Moderate hypothermia
28-32
Decreased LOC, cardiac disturbances, pupil dilation
decreased RR
27
Severe hypothermia
20-28
Complete CV and nervous system collapse (absent motor and reflex functions)
Cardiac standstill @ 20
28
Profound hypothermia
14-20
Cardiac standstill @ 20
29
Deep hypothermia
<14
30
Radiation
Occurs when heat passes from a warmer to cooler area through the air without direct contact
55-60% heat loss
31
Conduction
Transfer of heat through direct contact with cool objects
15% heat loss
32
Convection
Movement of air or liquids over the skin
33
Evaporation
Transfer of heat through moist skin/mucous membranes/wounds
30% heat loss
34
Cold diuresis
Fluid shifts from vascular to interstitial space, decreased ADH, decreased Na/H2O absorption
*Can't use UO as measure of EOP
35
Passive external rewarming
Hemodynamically stable, standard of care to increase temp 0.5-2 degrees/hr and prevent further heat loss
Warm blankets, remove wet clothes
36
Active external rewarming
Faster rewarming @ 1-2.5/hr
Convective air blankets/warm water immersion/radiant heat
37
Afterdrop
S/p direct rewarming, peripheral vasodilation results in transport of cooler peripheral blood to core, causing decreased temp
38
Rewarming shock
Decreased BP associated with vasodilation and volume depletion (cold diuresis)`
39
Active core rewarming
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)
40
Extracorporeal rewarming
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)
41
Rescue collapse
Cardiac arrest associate with
extrication and transport of a patient
with severe hypothermia
42
Bariatric surgery indications
BMI > 40 or BMI > 35 + comorbidity
43
Malabsorptive/restrictive
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
44
Restrictive
Gastric sleeve
Simpler procedure, can be revised to gastric bypass if needed
60% weight loss over 2 years
Common complication = strictures
45
Dumping syndrome
N/V, tachycardia, abdominal cramping, diarrhea after high sugar meals (esp common after Roux en Y)
46
Bariatric surgery complications (early)
PE
Gastrointestinal leak
Infection
47
Cirrhosis
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
48
Albumin
3.5-5.5
Colloid oncotic pressure, synthesized by the liver
Complications if low: 3rd spacing, ascites, edema, anascara
49
INR
Normal = 1
Vitamin K Dependent clotting factors (II, VII, IX, X) synth by liver
Complications if derangement: bleeding, bruising, prolonged PT
50
Plt
Low for 2 reasons in liver failure
1. TPO synthesized by liver
2. Splenomegaly d/t portal HTN = increased sequestration
Derangements = bleeding, bruising
51
AST
< 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
52
ALT
< 40
More specific for liver
Elevations indicate liver injury, steatohepatitis
53
Alkaline phosphate
<100
Found in biliary tree, bone, placenta
Elevated when obstruction in biliary tree
54
Bilirubin
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
55
Cholelithiasis
Gallstones, no issues
56
Biliary colic
gallbladder contracts and pushes
stones back and forth into the cystic duct, pain <6 hours associated with N/V (no fevers or chills)
57
Cholecystitis
biliary colic that does not resolve > 6
hours, causing inflammation, N/V/RUQ pain + fever
58
Choledocholithiasis
Gallstones in the common bile duct
59
Cholangitis
Gallstones in the CBD causing infection/fever and/or obstruction
60
Charcot's triad
Cholangitis: RUQ pain, fever, juandice
61
Raynaud's pentad
Cholangitis:
Charcot's triad (RUQ pain, fever, jaundice)
+
Hypotension
+
AMS
=
Very very sick, sepsis
62
Hepatocellular injury
AST/ALT > 40
+/- Indirect bili > 1
(out of proportion to elevations to Alk phos or D bili)
63
Cholestatic injury
Alk phos > 100
Direct bili > 1
+/- AST/ALT > 40
(Alk phos and D bili elevated out of proportion to AST/ALT)
64
HAV
RNA
Transmission: Fecal-oral
Vaccine: Yes
Cirrhosis risk: No
Tx: supportive
65
HBV
DNA
Transmission: Blood, body fluid, perinatal
Vaccine: Yes
Cirrhosis risk: Yes
Tx: Antivirals, supportive, close monitoring
66
HCV
RNA
Transmission: Blood, body fluid, perinatal
Vaccine: No
Cirrhosis risk: Yes
Tx: Antivirals
67
HDV
RNA
Transmission: Blood, *needs HBV to enter liver cell
Vaccine: Yes (HBV)
Cirrhosis risk: Yes
Tx: Antivirals, supportive, close monitoringR
68
HEV
RNA
Transmission: Fecal-oral
Vaccine: No
Cirrhosis risk: No
Tx: Supportive, pregnant people may develop liver failure
69
Ammonia
From protein metabolism by gut bacteria, cleared by the liver.
If not adequately cleared, accumulates and easily crosses BBB causing hepatic encephalopathy
70
AKI
Loss of GFR over hours to days, inability to excrete daily solute
71
Pre-renal azotemia
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
Obstructive uropathy (post-renal)
Causes: kinked foley, BPH, malignancy, anti-cholinergics, ureteral obstruction
Dx: bland UA, renal US
Tx: insert/flush foley, BPH meds, D/C anticholinergics
73
Acute tubular necrosis
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
Allergic interstitial nephritis
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
Acute glomerulonephritis
Autoimmune reaction in the kidney
Dx: RBC and RBC casts in urine, proteinuria, HTN, renal biopsy
Tx: immunosuppression, dialysis maybe necessary
76
Tetraplegia
Injury to cervical spinal cord causing loss of muscle strength in 4 extremities C1-T1
77
Paraplegia
injury to the thoracic spine (T2-T12)
78
ASIA A
Complete: No sensory/motor function, including sacral segments
79
ASIA B
Sensory recovery: Sensory but no motor below level of injury, sacral sparing
80
ASIA C
Motor recovery/non-functional: Motor function preserved below injury, but most key muscles unable to resist gravity (less than 3/5 strength)
81
ASIA D
Motor recovery/functional: Motor preserved below injury, most key muscles greater than 3/5 strength
82
ASIA E
Complete recovery
83
Posterior cord syndrome
Very rare, most often occurs with tumor invading cord (less often traumatic)
Loss of proprioception, ataxia. Maintain pain, temp, motor function
84
Central cord syndrome
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
Anterior cord syndrome
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
Brown-Sequard Syndrome
Very rare. Hemisection lesion of cord. Good prognosis
Ipsilateral loss of motor and proprioception
Contralateral loss pain/temp
87
Cauda equina
lumbarsacral nerve roots, affects bowel/bladder. Often caused by
lumbar disk herniation
88
Spinal cord concussion
transient neurologic deficit without any apparent structural damage
Common in young athletes, typically resolves within 48 hours
89
Neurogenic shock
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
Autonomic dysreflexia
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
GERD
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
H2 blockers (ranitidine, famotidine)
Can be taken on PRN basis (not recommended for GERD with complications) blocks initial part of acid secretion pathway
93
PPI (Omeprazole, Lansoprazole)
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
Barrett's esophagus
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
H pylori
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
Acute pancreatitis
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
Crohn's
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
Ulcerative colitis
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
Thrombocytopenia
< 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
Pseudothrombocytopenia
Laboratory artifact, usually due to EDTA-dependent antibodies
Solution: repeat CBC in a heparinized or sodium citrated tube
101
ITP
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
Drug induced thrombocytopenia
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
HIT
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
TTP
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
DIC
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
Calcineurin inhibitors (Cyclosporine, Tacrolimus)
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
Antiproliferative agents (CellCept, Myfortic)
Immunosuppressive agents: Prevent B and T cell proliferation
ADE: Myelosuppression (anemia), GI intolerance, pancreatitis
108
mTOR Inhibitors (Sirolimus, Everolimus)
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
Corticosteroids
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
Infection prophylaxis (Txp)
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
Txp adjunctive meds
Anti-HTN
Statins
BG management
GI prophylaxis
ASA
Pain management
Supplements: Vitamins, Ca, Mag, Iron
112
Hyperacute rejection
Blood or antibody incompatibility
113
Acute cellular rejection
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
Chronic rejection
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
Antibody mediated rejection
Antibodies form against donor tissue antigen
D/t inadequate immunosuppression
Can lead to severe graft dysfunction
Tx: plasmapheresis, IVIG, Rituximab
116
Kernig's sign
Severe stiffness of the hamstrings causes an
inability to straighten the leg when the hip is flexed to 90 degrees.
117
Brudzinski's sign
Severe neck stiffness causes a patient’s knees
and hips to flex spontaneously when neck is
flexed
118
Acute bacterial meningitis
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
Encephalitis
AMS, motor/sensory deficit, speech/movement disorders, personality changes
120
Meningococcal septicemia
Meningococcal meningitis when it becomes systemic
Loss of limb
Organ damage
DIC
Death
121
Tuberculous meningitis
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
Cerebral abscess
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
Spinal epidural abscess
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
Viral meningitis
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
Acute viral encephalitis
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
HSV encephalitis
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
Neurosyphilis
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
Argyll Robertson pupils
Pupils constrict with accomodation but not when exposed to bright light
129
Toxoplasmosis
Parasitic infection
Acquired from: perinatal, unwashed veg/undercooked meat, cat droppings
Tx: Sulphadiazine and pyrimethamine
with folic acid for 6 weeks
130
Prion disease
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
C-spine
Smaller bones require ligaments to hold together. Can have unstable/mobile spine in the absence of fractures/bone trauma
132
Primary injury (SCI)
mechanical disruption, transection, distraction of spinal cord (ie fractures, penetrating injury, hematoma or abscess, metastatic disease)
Goal is to prevent progression
133
Secondary injury (SCI)
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
Sacral sparing
Some signal still innervates sacral nerves (bowel/bladder). Does pt have rectal tone? IF yes, incomplete/better prognosis.
ASIA B-E
135
Intubate? (SCI)
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
MAP Goal SCI
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
VTE Prophylaxis (SCI)
LMWH initiated w/in 72 hours (pending ESS approval) -- 3 months/rehab phase
138
Transplant Complications
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
Kidney txp
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
Liver txp
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
Heart txp
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
Lung txp
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
Hypothermia complications
Rescue collapse
Pulmonary edema and acute resp failure after rewarming
Multiorgan failure
Consider targeted temperature management 24 hr
144
Endpoints to resuscitation (hypothermia)
Hyperkalemia >10
pH < 6.5
Severe coagulopathy
Persistent asystole despite temp >32
145
Metabolic response hypothermia
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
CV response hypothermia
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
Pulm response hypothermia
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
Neuro response hypothermia
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
GI response hypothermia
Decreased motility/liver function/insulin release from pancreas
Ileus
Bacterial translocation
Stress ulceration
150
Heme response hypothermia
Plt dysfunction
Enhanced fibrinolysis
Alterations in enzyme function
Increased blood viscosity
Hemoconcentration
Critical coagulopathy @34
151
AST/ALT >1000
Tylenol toxicity
Viral hepatitis
SHOCK liver
HELLP
Budd-Chiari
Autoimmune
152
SHOCK liver
Hypoperfusion liver injury
Sepsis
Hypovolemia/Hemorrhage
Obstruction
Cardiogenic
Kombos of the above
1 cause of AST/ALT > 1000
