2 Flashcards
Fulminant (acute) liver failure
Rapid development over <26 weeks, usually in a previously normal liver
Mental status changes and elevated INR required for Dx
More common in young people, ass. w/ high M&M
Common etiologies: drug induced (acetaminophen), viral, autoimmune, shock
Acute on chronic liver failure
Underlying liver disease + acute decompensating event (bleeding, infection, ascites, encephalopathy)
Leads to worsening liver failure and other organ failure
Very high short term mortality
Chronic liver disease
Accounts for majority of cases
Progressive fibrosis over many years
Often asymptomatic (compensated) –> decompensation leads to manifestations of liver failure
Potential for reversal in some cases
Portal hypertension
- Increased hepatic resistance to portal inflow d/t architectural distortion and intrahepatic vasodilation from cirrhosis
- Increased splanchnic vasodilation from excess NO and vasodilators
Pressure > 5 mmHg seen in 80% cirrhosis patients
Pressure >10 mmHg = clinically significant, decompensated
Pressure > 12 mmHg = threshold for bleeding varices
Ascites
Most common complication of cirrhosis/most common cause of hospital admission
Portal hypertension –> increased hydrostatic pressure/decreased oncotic pressure from albumin
AND splanchnic vasodilation –> effective hypovolemia –> RAAS activation –> Na/H20 retention
Hypervolemia + decreased oncotic pressure
Management: 2 G Na diet, diuretics (furosemidse 40 mg, spironolactone 100 mg), paracentesis, TIPS procedure
SAAG
Serum albumin – ascitic albumin
If > 1.1, ascites likely caused by portal hypertension
NEXT STEP: ascitic protein
Ascitic fluid data
Cell count/differential
Albumin
Total protein
+/- cultures
+/- glucose
+/- lactate
Ascitic protein
<2.5 indicates ascites from cirrhosis, late Budd-Chiari syndrome, liver mets
Spontaneous bacterial pleuritis
PMN > 500
> 250 in ascites fluid or > 250 w/ +bacterial culture in lung fluid
Varices
Body’s attempt to find alternative roads back to heard
Thin, fragile walls which can easily reach critical point of pressure and burst (size of varices proportional to bleeding risk)
Acute bleeding event typically lasts 5 days, but risk of rebleeding
Ceftriaxone, octreotide, nonselective beta blocker
TIPS
Reduce HVPG <12, open up new roads to liver by placing stent through inflow/outflow of liver connecting one branch of portal vein to hepatic vein
Contraindications: HF, uncontrolled infection, biliary obstruction, severe pulm HTN, thrombocytopenia
Complications: encephalopathy, decomp HF, liver failure, infections, bleeding
Hepatic encephalopathy
stage 1. subtle personality changes, decreased attention
stage 2. lethargy, disorientation, asterixis,
stage 3. stupor, severe confusion, incomprehensible speech
stage 4. coma
from increased ammonia crossing BBB –> edema of brain and astrocyte swelling
Don’t trend ammonia to monitor clinical response in chronic liver failure, but may be helpful in fulminant
Tx: underlying cause (infection, dehydration, electrolyte imbalance, bleeding), lactulose, rifaximin
Hepatorenal syndrome
Only seen in presence of advanced portal HTN w/ ascites, corrects after liver txp
Increased blood into portal circ/increased NO, decreased PVR, activation of RAAS =renal vasonconstriction/decreased renal blood flow
Child Pugh Score
Objective criteria (bili, INR, albumin) + subjective criteria (encephalopathy, ascites)
Class A-C. Class C eval for Txp
STI Screening Recommendations (CDC)
Gonorrhea-yearly for patients at risk/in high burden communities
Chlamydia-yearly for women <25 or w/ multiple risk factors
Syphilis-yearly for MSM or w/ multiple/anonymous partners. Twice during pregnancy
HIV-all adults and adolescents screened at least once
W/ any new STI Dx, also screen for HIV, Syphilis, Hep C (and retest at 2-3 months)
Genital ulcers
painful = genital herpes
painless = syphilis
all ulcers should prompt screening for syphilis
also think monkeypox
Primary syphilis
incubation: 10-90 days
starts w/ chancre (early macule/papule, then erodes)
resolves in 1-6 weeks
highly infective
Tx: PCN G (Ceftriaxone if PCN allergy)
Secondary syphilis
2-8 weeks after chancre, spirochetes have disseminated
Painless rash on whole body, including hands and feet
-mucous patches
-condylomata lata
-constitutional symptoms
-lymphadenopathy
Tx: PCN G weekly x3 for late latent
Tertiary syphilis
Does not always develop in untreated syphilis, can take 10-30 years to develop
Involvement = neuro, cardiac, eyes
Neurosyphilis can occur at any stage: CNS dysfunction, meningitis, AMS, stroke
TX: Aqueous PCN G IV q4 x2 wk
Genital herpes (HSV 2)
transmission: direct contact (can occur w asymptomatic shedding)
primary infection can be asymptomatic, symptomatic infections may be severe and prolonged
complications: neonatal exposure, enhanced HIV transmission
Sx: buzzing sensation, painful vesicles/ulcerations/crusting
Dx: NAAT, culture and PCR
Tx: Acyclovir/Famciclovir/ Valacyclovir 10-14 days
First episode, episodic, and suppressive therapies
HPV
associated with cervical cancer, genital warts and some oral/anal/penile cancers.
risk factors: old age, immune suppression, non-circumcised men, multiple partners, persistent infection
HPV 16 and 18 responsible for 80% cervical cancers
Cervical cancer screening
Screening should begin at 21 years of age
Age 21-29 years= Cytology alone
Age 30-65 years – Anyone of the following
Cytology alone every 5 years
FDA approved hr HPV testing along every 5 years
Co testing for hr HPV and cytology every 5 years
Over 65- No screening after adequate negative
Hysterectomy with removal of Cervix- no screening
if there is no history of high grade cervical
precancerous lesion or cervical cancer
Genital warts
HPV 6 and 11 cause 90% of genital warts
Incubation: 3 weeks–months
Sx: bumps, itching, irritation,
burning (or may be asymptomatic)
Gonorrhea
Causative organism: Neisseria Gonorrhae
Incubation: 2-5 days
Treatmnt for both partners is essential, treatment resistance on the rise
Sx (Males)- dysuria, discharge, disseminated can cause rash/joint pain/endocarditis
Sx (Females)-majority asymptomatic. discharge, dysuria, labia pain and swelling
Dx: NAAT (urine, cervical, urethral testing)
Tx: Ceftriaxone 500 mg (1 G if pt > 150 kg) + Doxycycline if chlamydia not excluded
Suspect tx failure if sx do not resolve w/in 3-5 days after tx: ensure pt has had no sexual contact and test for cure
Notify health department for tx resistant
PID
usually caused by gonorrhea/chlamydia
Sx: pelvic/abd pain, abnormal vaginal bleeding, dyspareunia, fever, cervical motion tenderness, adnexal tenerness
Dx: purulent cervical discharge, elevated ESR
Tx: Ceftotetan or Ceftriaxone and Doxy
Chlamydia
Most common in adolescent females, high rate of reinfection
Risk factors: age, gender, # partners, mucopurulent cervicitis, Hx STIs
Sx (Males) often asymptomatic, tingling in urethra, discharge
Sx (Females) vaginal discharge, cervical friability, poorly differentiated abd pain, bleeding after intercourse
Complications: infertility, increased risk ectopic pregnancy, chronic abd pain, premature ROM, low birth weight, conjunctivitis, blindness in infants
NAA testing, pt collected swabs
Tx: Doxy 7 days (Alt: Levo) If compliance is an issue Azithromycin
Trichomonas
flagellated protozoan
resistance escalating, infections can last months-years
Sx: malodorous discharge, burning/pruritis/urinary frequency
chronic infections may be asymptomatic
Associated w/ premature ROM, low birth weight, preterm birth
Tx: Metro 500 BID x7 days
Bacterial vaginosis
polymicrobial clinical syndrome resulting from
replacement of the normal hydrogen peroxide
producing Lactobacillus sp. in the vagina with
high concentrations of anaerobic bacteria
Increased risk for other STIs
Tx: Metro 500 mg BID x7d
Multiple sclerosis
Immune mediated, chronic inflammatory disease of CNS
Hallmarks inflammation, demyelinating plaques, axonal loss in CNS triggered by autoimmune mech
Risk factors: Age (predominantly female), geography, sun exposure, EBV, cigarette smoking, high dietary salt intake
Sx: acute optic neuritis, partial transverse myelitis, bladder/bowel sx, vertigo/impaired balance, banding around trunk (MS hug), Lhermitte’s, Uhthoff’s
Dx: Clinical Sx + MRI of brain, cervical/thoracic spine w/wo contrast, labs to r/o mimics , LP, evoked potentials
Lhermitte’s phenomenon
Tingling down the back and into the shoulder when flexing neck
Uhthoff’s phenomenon
MS symptoms are worsened by increasing body temp
Relapsing-remitting
No new disability between flares
Primary progressive
Steady increase in disability w/o attacks
Secondary progressive
No new disability btwn attacks, followed by steady increase in disability
Interferon beta
Promote shifts from T-helper (Th)1 to Th2.
Pegylation is the addition of polyethylene glycol and is thought to increase the potency and half life of interferon beta.
ADE: Injection-site reactions, flu-like symptoms, mood changes.
Glatiremer acetate
Copolymer originally designed to mimic
myelin basic protein in animal studies
Promote differentiation into Th2 and T-reg cells
ADE: injection site rxn, post injection tachycardia
Safe for use in pregnancy
Fingolimod
S1P1 receptor
modulator, prevents lymphocyte migration from
lymph organs into peripheral circulation
ADE: 1st dose bradycardia, infections, macular edema, worsening PFTs
Contraindicated w/ beta blockers, check for hx skin cancer and heart/pulm disease
No live vaccines while receiving this med
Teriflunomide
Blocks the replication of rapidly dividing T- and
B-lymphocytes
Monitor for GI/liver abnormalities, hair thinning
Teratogenicity
Dimethyl fumarate (DMT)
Promotes anti-inflammatory and cytoprotective
mechanisms
ADE: GI sx, flushing, lymphopenia, risk of infection
Monoclonal antibodies
Natalizumab: binds
α4-intergin on lymphocytes, preventing their interaction with vascular adhesion molecules –> reducing migration into CNS
ADE: opportunistic CNS infections
Alemtuzumab: against CD52 that results in lymphocyte depletion
ADE: infections, secondary autoimmune, malignancies
Ocrelizumab: against CD20 receptors on B-cells
ADE: injection site rxns
No live vaccines on this therapy
DMT injectables
Monitor CBC, liver enzymes annually
Considered safest in tx of MS
Can get live vaccines on this therapy
Some safe in pregnancy
DMT Orals
Monitor for infection (ass. w lymphocytopenia)
No live vaccines before consulting neurologist
Monitor LFTS
Most teratogenic
MS Relapse
Acute episodes of new or increasing neuro dysfunction, followed by full/partial recovery.
(In the absence of fever or infection)
New sx of neurological dysfunction, in a new
area of the body, lasting more than 24-48 hours
consistently.
(Not attributable to another cause such as infection or
other cause (not a pseudo-exacerbation).)
Pseudo-exacerbation
Flare up of old symptoms caused by trigger: infections, stress, sleep deprivation, heat sensitivity, healing wounds from surgery, pre-menstrual time.
Tx: if infection present treat infection, steroids are
usually contraindicated in these instances. Address root
cause
Hs&Ts
Hypovolemia
Hypoxia
Hypothermia
Hypo/Hyperkalemia
Hydrogen ion
Tension pneumo
Tamponade (cardiac)
Toxins
Thrombus (pulm, cardiac)
NULL-PLEASE Score
Nonshockable rhythm
Unwitnessed arrest
Long no-flow period (no bystander CPR)
Long low-flow period (>30 minutes before ROSC
pH (arterial) <7.2
Lactate >7 mmol/L
End-stage kidney disease on dialysis
Age ≥85 years
(Still) Ongoing CPR on arrival to hospital
Extracardiac cause
Patients with ≥5 features on the NULL-PLEASE score had a greater than threefold risk of
mortality compared with patients with a score from 0 to 4
CREST Score
Coronary artery disease (preexisting)
Rhythm nonshockable
Ejection fraction <30 percent
Shock at presentation
Ischemic time prior to ROSC >25 minutes
Risk of circulatory death increased with every additional point, from 10 percent
mortality with CREST = 0 up to 50 percent mortality with CREST = 5.
TTM
To improve neuro outcomes for comatose pt post cardiac arrest:
Inhibits cell death by reducing glutamate
release, decreasing concentrations of
intracellular ca, inducing anti-apoptotic factors and suppressing propoptotic factors
Oxidative injury and global cerebral inflammation also decreased
Decreased cerebral metabolism by 6-7% by 1C, also decreases blood flow and ICP
Cooling to 33C = 25% reduction in metabolism
Implementing TTM
All comatose pt post cardiac arrest (regardless of initial rhythm/location of arrest) up to 12 hr-post ROSC
Exclusions:
GCS >6
Severely impaired cognitive state prior to arrest
Sustained non-perfusing rhythm
DNR
Target temp: 33 (36 if bleeding risk)
Sedation/analgesia: propofol./fentanly
Consider NMB to prevent shivering
Continuous temperature monitoring device req
TTM considerations
Glucose/electrolytes: cold diuresis, replete as needed. caution of extracellular shifts during rewarming, caution in renal failure. avoid K containing fluids but check BMP Q6 and replete as needed. Hyperglycemia during hypothermia may req insulin gtt but caution for hypoglycemia during rewarming
Shivering: EKG and EEG to watch for micro shivering. NMB, tylenol, BuSpar, Mag, and analgesia/sedation
CV: Myocardium less response to defib and meds <30C, need hourly VS and art line for BP, repeat EKG @ target temp, dysrhythmias more common <30
Pulm: hyperoxia associated w/ worse outcomes. Goal SpO2 90-96%
Neuro: Q2 h neuro checks and cont. EEG 12 hours after initiation
Adrenals: Often see adrenal insufficiency post-resusc. Stress dose steroids recommended in refractory shock
Active normothermia 72 hours post rewarming (Cooling packs and tylenol)
Epidural hematoma
Bleeding between dura mater and skull
Mostly from arterial injury
Lens shaped
Subdural hematoma
Bleeding between dura and arachnoid space
Rupture of bridging veins
Crescent shaped
Traumatic subarachnoid hemorrhage
Tearing of small vessels in pia mater
Diffuse axonal injury
Tissue shearing at gray/white matter junctions
Visualized only on MRI
Skull fractures
Linear–most common, usually non-emergency. Temporal fx = risk of seizures
Stellate/comminuted–multiple associated linear fx
Depressed/penetrating–pressure causes injury, neuro signs evident. Req surgical repair, seizure prophylaxis and abx
Basilar–Difficult to see on XR, Dx by Sx (raccoon eyes, battle sign, CSF otorrhea/rhinorrhea)
Monroe-Kellie Doctrine
After TBI, any of the intracranial compartments can expand w/in fixed space (skull) leading to increased pressures
Brain parenchyma
CSF
Blood
Indications for surgery
Hemorrhagic lesions (evacuation and decompressive craniotomy)
-midline shift >5mm
-expanding hemorrhage or >10 mm
-GCS <8
Intracerebral contusions
-If refractory to medical therapy
Chronic SDH (Burr hole + subdural drain)
Herniation S/Sx
ipsilateral dilated pupils, Cushing reflex (HTN, bradycardia, resp depression), cortical blindness
ICP
Goal < 22
Clinical exam: herniation, Cushing reflex
Invasive monitoring: Intraventricular (Gold standard), Intraparenchymal (Bolt), Subarachnoid, Subdural
ICP Waveform: P1>P2 in normal, compliant cranium. P2>P1 indicates high pressure, noncompliant
Tx Elevated ICP
Tier 1
1. Optimize venous drainage: position HOB @ 30, keep head midline, remove C collars. Decrease metabolic demand: sedation/analgesia, seizure/fever prophylaxis, TTM
Tier 2
2. Slight hyperventilation
- CSF Fluid diversion
- Hyperosmolar therapy (brain edema therapy): mannitol vs. hypertonic saline
Tier 3
5. Salvage therapies: decompressive hemicraniectomy, laparotomy, neuromusc paralysis
Mannitol (sugar alcohol)
Filtered in kidney causing diuresis of Na/H20 –> TOTAL BRAIN & BODY DEHYDRATION
1g/kg Q6 H. Replete urine 1:1 for 2 H post admin
Monitor renal function, BMP, serum osmolarity
Not for renal failure
Hypertonic saline (3%, 5%)
No diuretic effect, so can be used in renal dysfunction
Expands intravascular volume and CO
Initial bolus, followed by infusion
Trend Na, stop when Na>160
Brain tissue oxygen
Partial pressure of O2 in brain interstitial space available for oxidative energy production
Determined by cerebral blood flow and arterial O2 content
Monitoring = regional or global
SjvO2
Global monitoring: Jugular bulb catheter measures O2 sat in jugular vein
Normal: 60-70% (Danger <50%)
Decreased SjvO2 = inadequate delivery of O2 relative to demand
Increased SjvO2 = delivery > metabolic requirements
pbtO2
Regional monitoring:
Licox measures the partial pressure of O2 in brain interstitial tissue
Normal pbtO2 range 25-50mmHg
Cerebral autoregulation
Maintains cerebral blood flow at a constant, despite fluctuations in cerebral perfusion pressure.
Determined by resistance of the cerebral blood vessels (diameter)
Disruptions seen in trauma and stroke–>Even minor changes in CPP can result in significant changes to blood flow
