Plans
Neurological System
Headache
-Mg + reglan is a good cocktail
Neuro BP Goals
-Bp less than 180/105 for post thrombectomy
-BP < 185/110 mmHg is required for IV tPA eligibility. After infusion has begun, a goal of < 180/105 mmHg should be maintained for 24 hours.
ACUTE STROKE ENLS
(clinical dx, cnt ddx ischemic vs hemorrhagic by exam. Look for hyperdense MCA sign on CT. hypodensity will not show on ct scan until about 6hrs. >1/3 of cerebral hemisphere is contraindication to tpa
-communication/question to ask on signout
1.LKW
2.NIHSS- tells you risk of ICH after tpa. 11-20 =5%, >20=17%
3. occlusion location, ASPECT score(for MCA strokes CT imaging prognosis. score less than or equal to 7 predicts a worse functional outcome at 3 months as well as symptomatic hemorrhage)
3.5 tPA or no tpa?
4.TICI score
5. BP goal
6. if on ACs antiplts, determine last time hrs were taken
-BP checks q15 x2hrs then q30 x6hrs > q1hr x16hr>
-q1hr neuro checks
-No anticoagulation/antiplatelet therapy x24hrs post tpa
-keep pt euvolemic with ns
-glucose level 140-180
-agrressive tx of fever
-avoid foley Cath, ng tube, intra-arterial catheters for 4 hours after tpa administration
-Document tici score, NIHSS, ASPECT
-pts not getting tpa can have permissive hypertension
Post tPA management
- tPA dose is 0.9mg/kg. max 90mg. .given 10% bolus in one minute then the rest can be over 1hr
-give cryoprecipitate if pt deteriorates after tpa(6-8units). Platelets and antifibrinolytics may also be considered.
-Neuro check q1hr
-Bp < 180/105 for post thrombectomy
-BP < 185/110 mmHg is required for IV tPA eligibility. After infusion has begun, a goal of < 180/105 mmHg should be maintained for 24 hours.
Cthead 24hrs post tpa and then as needed if worsening neurological status
Brain mri
Tte
30 days cardiac monitoring at discharge, lipids profile, a1c, troponins
Follow up with neurology
Asa/artovastatin
EVERY post stroke pt needs SLP
TIA PLAN:
The ABCD2 score predicts risk of subsequent stroke following a TIA based on patient demographic and clinical features. For low risk patients (scores 0-3) an outpatient work-up in the 1-2 days following score calculation may be appropriate. It is recommended to start an antiplatelet agent and a statin.
Start antithrombotic agent - ASA, clopidogrel, ASA/dipyridamole
Start high-intensity statin (consider moderate intensity in age >75 yrs)
Carotid imaging (ultrasound, CTA, MRA)
Consider transthoracic echocardiogram
Consider 30-day ambulatory cardiac monitor
Encourage smoking cessatio
IntracranialHTN ENLS | Elevated ICP
-first line TXs: hyperomsmolar therapies (23%NaCl 30mLs q6h, Mannitol 1g/kg up to 90g), hyperventilation, CSF drsinsge(EVD), consider surgical decompression.
-Evacuate mass or lesion if there
-More sedation including pentabarb
sICH ENLS (hemorrhagic stroke)
-Causes: htn, CAA(lobar hemorrhages), coagulopathy(on AC/antiplts), vascular anomalies, sympathomimetic drugs(cocaine. Methaphetamines)
-These pts will have intact GCS then drop suddenly
-cerebellar or temporal bleeds most at risk for herniation
-ICH score >2 is dangerous hemorrhage
-suspicion of ICH > adequate airway?(intubate) > CTnoncon
-communication: ABCs, gcs, lkw, hx of stroke/blood thinners/bleeding,current meds,coags,
-characterize ich score, volume, location, ivh present?,GCS
-SBP goal <140-180mmHg (use labetalol, nicardipine or clevidipine gtts)
-INR <=1.4 (consider reversal agents, DDAVP/PLTs if surgery planned)
-can reverse warfarin coagulopathy with vitk 119ng iv and PCC>ffp. Dose based on inr
-Consider surgery for evacuation
-Consider EVD(goal icp<22, cpp>60)
TBI(EDH/SDH/DAI/diffuse cerebral swelling/Contusions/SAH/IVH ENLS
-Communication=pre injury baseline, home blood thinners, mechanism/time of injury, LOC?/szr?/helmete?, post tx gcs + eye exam, cth results, Cspine status, other injuries, labs, tx given, nsg plan
-SBP goa>110mmHG. >100 if 50-69 yrs old
-Look at ENLS slides for who goes to neurosurgical intervention
-Look at slide for herniation syndromes
-GCS 12 or less =ICU
-CTh, +/- cta head/neck, ct c-spine
- consider C-collar, C spine precautions
-NSG following
- avoid hypoxemia, hypotension
- monitor ICP, signs for herniation
- correct Coagulopathy
- Seizure prophylaxis x7days
- avoid hyperventilation, steroids, hypothermia
-Can do TTM for down to 32cc
Meningitis/Encephalitis ENLS
-Start BS ABXs > CTh then LP
- https://onedrive.live.com/view.aspx?cid=B383FB7D24B0D769&resid=B383FB7D24B0D769%212791&canary=O0QWWeI0za4djvB6pPhHwbNvadKMLJ0jO%2BO4iM6f2tU%3D0&ithint=%2Epdf&open=true&app=WordPdf
-dont delay ABXs
-get CT before lp because if they have cerebral edema and you drop their ICP by taking out volume, you can lead to herniation.
-if suspecting HSV add acyclovir. add ampho b if immunocompromised pts.
-LOOK at slide about lp labs to send and normal levels
-herpes encephalitis will have FLAIR abnormalities on mri
SE ENLS
-Etiology(Acute causes include metabolic disturbances, renal failure, sepsis, CNS infection, stroke/tbi, medication NON ADHERENCE/intoxication, or withdrawal from BZD, barbiturates, etoh or other sedatives, cardiac arrest hypoxia, hypertensive encephalopathy.
Chronic (Chronic causes include epilepsy, chronic IDE abuse, CMS tumors, remote CNS pathology IE strokes, abscess)
-initial work up in ED consider CT/MRI or LP if infection suspected
-make sure glucose checked
-SE is a continuous emergency
-the sooner you can treat them the higher chance of recovery you have
--1st line= Lorazepam 0.1mg/kg IVP FIRST LINE>up to 4mg per dose x2doses. Midaz IM 10mg if >40kg weight, 5mg if less< 40.
-2nd line= phenytoin, fosphenytoin, phenobsrb, keppra
-keppra is second line
-remember to not under dose pts in SE
-Diazepam 20mg rectal is also option if no IV access
-if given 1st line after 10-20mins still in SE, then give 2nd line=fospheny 20mg/kg vpa 40mg/kg, kepp 60mg/kg(max 4500mg)
if 2nd line has failed=REFRACTORY SE=LOOK AT SLIDE with doses
- lamotrigine and Keppra lower risk of teratogenicity than vpa, pheny--have to check drug levels.
cEEG is necessary in SE even if the clinical seizures have stopped
Use Valium since it is longer acting with lower chance of recurrent withdrawal or seizures.
Preferably to use Ativan in patients with advanced cirrhosis or acute alcoholic hepatitis.
aSAH management
-CTA does not rule out aneurysmal sah. need to get 4vessel.
-better to wait to get LP if suspecting SAH. good to wait 6hrs.
-look at slide for LP findingsf
-SAH has alot of cardiac complications: arrhythmias, takatsubos, neurogenic pulmonary edema
-goal INR<1.4 reverse warfarin with some combo of ffp/k/or PCC.
-goal plts>50,000
-consider plt transfusion for those on anti platelet meds
-NSG consult
-SZR ppx
-tx pain with IV short half life meds (fent)
-lorazepam small doses for anxiety
-sbp<160 or map<110
-use short-acting, titratable iv blockers or nicardipine
-avoid long term nitroprusside
-consider txa or caproeic acid for ppl prophylaxis
-document mRs, hunt & hess(grades0-5,5 worst looking at initial exam. An index of prognosis though not fully accurate especially with lower scores), fischer grading scale(index of the risk of delayed cerebral ischemia due to vasospasm after sah. Grades 0-4, 4worst).
-in SAH maintain euvolemia and normal circulating blood volume to prevent DCI(delayed cerebral infarction)
- these pts are susceptible to hyponatremia
-if nimodipine causing low bp, can d/c it.
-Have to get TCDs(transcranial dopplers)
TSI
-In general pts with complete TSI above C5 should be intubated ASAP
-should intubated using awake fiberoptic intubation vs in line stabilization
-bp goal is map 85-90 x7days
-Neurogenic shock duration can be 1-3wks and can be late(hours or days after injury)
-Spinal shock(not to be confused with neurogenic shock) has nothing to do with hemodynamics= refers
- Neurogenic shock is the loss of sympathetic tone, which leads to vasodilation and distributive shock, with hypotension and bradycardia. The skin remains pink and warm due to loss of sympathetic tone, and the body is unable to redirect blood flow from the periphery to the core circulation. to the loss of spinal reflexes below level of injury.
-use norepi as primary agent. Phenylephrine 2nd but can cause rebound bradycardia
TX
-decompression of cord(surgery), stabilization surgery, minimizing 2ndary complications
-tx neurogenic bladder
-Stress ulcer & VTE
-Steroids are not recommended
NEXUS criteria
1) Signs of intoxication, including the smell of alcohol on the patient.
2) Focal neurological deficits.
3) Painful distracting injuries, such as large bone fractures or lacerations, de-gloving or crush injuries, large burns, visceral injuries, or injuries that prevent functional ability.
4) Abnormal level of alertness.
5) Posterior midline tenderness to palpation.
ASIA CRITERIA
In ASIA Impairment Scale, AIS A is worst and AIS E is best.
AIS A is complete: No motor or sensory function preserved in the lowest sacral segment.
AIS B; Incomplete: Sensory function, but not motor function is preserved in the lowest sacral segment.
AIS C is incomplete; Less than ½ of the key muscles below the neurological spinal level have grade 3 or better strength.
AIS D is incomplete: At least ½ of the key muscles below the neurological level have grade 3 or better strength.
AIS E is normal: Sensory and motor functions are normal.
SPINAL CORD COMPRESSION ENLS
Definitions: neuropathy=peripheral nerves, myelopathy=spinal cord, radiculopathy= roots
Sx: acute or progressive weakness(paraplegia or quadriplegia), sensory changes, sphincter dysfunction. Hematomas can present with para or quadriparesis, pain worse when pt lies down. Disc herniation will cause (localizable radiating pain, loss of sensory or motor function, pain is worse when standing or sitting, better when in recumbent position)
Causes: Trauma, malignancy, infection, degenerative spine disease, hematoma, intrinsic lesions of the spinal cord, spinal cord ischemia
Workup: MRI modality of choice. If CI then CT myelography
lung, breast, prostate, rcc, lymphoma are common metastasis to spine.
myelopathy causes= trauma, malignancy, infection,
Disc herniation usually causes radiculopathy, acute myelopathy is rare
Rare for metastatic tumor to cross disc spaces. So Mri showing 2 contiguous disc spaces usually represents infection.
Tx:
-Determine level likely impacted (if pt upper extremities affected then suspect cervical lesion, pay attention to airway, breathing, Hemodynamics. If LE impacted, then lesion likely in thoracic spine)
-Spinal cord compression not due to trauma, bp goal is normotensive due concern the compression may be caused by hemorrhage
-Consider cervical collar
-Obtain NIF/FVC if warranted
-Tx for neurogenic shock if suspected/warranted
-give steroids in malignancy as cause of myelopathy
-Rad/Onc consult
-NSG/Ortho spine consult for surgical evaluation
-Pain control
-for infection/abscess: start vanc/3rd-4th gen C sporin, consider anerobic coverage with Flagyl check ESR, Bcx
-ESR<20 likely excludes spine infection
-for hematoma: Reverse coagulopathy
-Spine decompression
Anoxic Brain injury
-consider repeat cth/mri 48hrs from first to reassess anoxic brain injury
-keppra or depakote or clonidine for myoclonic jerks
-myoclonus within 24hrs is poor prognostic sign
Baclofen pump Withdrawal
Intrathecal baclofen: Abrupt withdrawal of intrathecal baclofen has been associated with altered mental status, exaggerated rebound spasticity, high fever, and muscle rigidity (which in rare cases has advanced to rhabdomyolysis, multiple organ-system failure, and death)
Oral baclofen: Abrupt withdrawal of oral baclofen has been associated with altered mental status, exaggerated rebound spasticity, hallucination, high fever, hypertension, hyperthermia, muscle rigidity, tachycardia, and seizure. Other symptoms include agitation, confusion, delusions, insomnia, and paranoid ideation
-sx are increase spasticity, AMS,/come, high fever, SZR, hallucinations, distributive shock, organ failure, sx can show up 48hrs after discontinuation of drug, can
-tx po baclofen, lorazepa,, q1hr neuro checks
-Baclofen down regulates GABA so thts why you treat with BZDs in withdrawal, can also try propofol
-Can consider cyproheptadine to mitigate serotonergic syndrome effects
- Dantrolene may be considered as an adjunct in patients with extreme muscle spasticity refractory to other therapies.
-Can consider tizanidine to manage spasticity
Hepatic encephalopathy
-precipitant of HE in cirrhotics include BZDs, zolpidem, narcotics, alcohol, increased ammonia production from excess protein, G.I. bleed, infection, electrolyte imbalances, constipation, metabolic alkalosis. Can also be from dehydration from v/d, hemorrhage, diuretics, large volume paracentesis, hepatic/portal vein thrombosis.
-avoid dehydration
- electrolyte abnormalities
-protein restriction only if protein intolerant
- lactulose 20–30 mg 2 to 4 times a day
- lactulose enema if no access
- rifaximin 550 mg bid or 400MG TID
PNES (psychogenic nonepileptic seizures)
-not associated with abnormal neuronal activity or reduced perfusion to the brain, has a female predominance
-sx(eyes are usually closed, often back to alertness quickly, can have incontinence, bite to tip of tongue
-Psychiatry consult
-antiseizure meds should be gradually withdrawn
-pharmacotherapy not effective
-CBT can be trialed
OPIOID USE DISORDER
-presenting s/sx may be of opioid withdrawal (eg, dysphoria, restlessness, rhinorrhea, lacrimation, sweating, myalgias, nausea, vomiting, abdominal cramping, and diarrhea
-A substance use history should include the amount, frequency, and duration of opioid use, last use, and signs of tolerance, and use of other drugs and alcohol
-Physical examination can detect signs of opioid use (eg, track marks, deviated nasal septum), as well as physical consequences of use (eg, infections and liver dysfunction
-Laboratory evaluation should include screening for HIV and hepatitis A, B, and C. Vaccination for hepatitis A and hepatitis B should be given to those with negative serologies
-GOLD STANDARD=urine drugs of abuse. Urine drug tests can detect metabolites of heroin and morphine within three days of last use and possibly longer in chronic users
-Most successful patients remain on maintenance treatment with an opioid agonist for many years, while a minority may be tapered off of agonist therapy after a few years
-tx/maintanance=methadone or buprenorphine.
Depression/Anxiety
PHQ9-used to screen for depression, can be used once a yr for pt wo depression(decreased enjoyment, feeling dow, low energy, low appetite, concetration, moving slow, si thoughts, in past 2 weeks
-score >5 uquals atleast mild depression may be there. thought you have to ask additional questions to see if depression is present.
- u say we just want to check how your
Managing Suicidality
-Have to know your resources ahead of times
-have to request emergent psychiatric eval
-call to take pt to ER
Orbital Cellulitis
-*Ophthalmologic emergency
-Other consultation as needed (e.g., ENT, neurosurgery)
-Immediate ophthalmology consultation
-Parenteral antibiotics against Staphylococcus species (especially MRSA) and Streptococcus species
Ceftriaxone and vancomycin (and consider metronidazole)
Respiratory System
ARDS plan
Dx- berlin criteria(known pulm insult<1week, b/l opacities on cxr/ct, noncardiogenic pulm edema(BNP<100, normal ef/function pcwp <15 though these aren’t fully reliable) and nonfluid overload(fluids, transfusions), P/F ratio<300)
- ARDS. Mechanical ventilation protocol.-ARDSNET
- Serial ABGs/CXR as needed.
- Aggressive pulmonary toilet, suctioning as needed.
- Not a candidate for SBT at this time.
- RASS target goal -4, +/- paralytic to optimize ventilator synchrony
- Consider/continue proning.(stop after 2wks if not responsive)-PROSEVA
-consider early referral for ecmo
-Consider flolan/nitric oxide.
-Scheduled/prn nebs
-Consider draining effusions if present
-Corticosteroids in ARDS is a conditional suggestion-meaning may be appropriate in certain pts-per 2024 ATS guidelines. Steroid increased risk of harm if using 2 weeks into disease
-VV-ECMO-conditional suggestion to use due to low certainy of evidence. ALWAYS use the other interventions first(proning, NMBs etc) -EOLIA
-In ARDS if you increase peep, and pplat goes down or stays the same, that means you recruited more lung. If pplat increases, that means you havent recruited more and might be overdistending.
-NMB-conditional reccomendation, low certainty. Recommended to be used early <48hrs. Also consider stopping after 48hrs or sooner. -ROSE ACURASYS
-PEEP-suggest using HIGHER peep without lung recruitment manuevers-conditional recommendation, low-moderate certainty. But reevaluate use of higher peep if clinical response to higher peep worsens, is deletrious
COPDAE(change in patients baseline dyspnea/cough/sputum production)
-causes can be infection, more smoking, acute PE(could even be subsegmental)). Subclinical PE
-Document PFTs, Home oxygen/Cpap/Bipap settings, Prednisone, frequency of hospitalization, outpatient Dr.
-bronchodilator therapy with albuterol(if no tachyarrhythmia), or Duo neb
-steroids x7-10days
-ABXs x5-7days
-In COPDAE, no need for Azithromycin if giving CTX.
-Bblocker use associated with excarcerbation-BLOCK-COPD
PNA
-Document site, Whether recurrent or new, clinical symptoms, last hospitalization, antibiotic exposure specially most recent used
-CAP—use CTX and Azithro
-HAP—Zosyn + Vanc
-Consider steroids (CAPECOD trial)
NON TB Mycobacterial infections including MAC
-generally free living organisms that are ubiquitous in the environment
-MAC is the most common cause of pulmonary disease among NTMs.
-sx: cough dry or productive, fatigue, malaise, weakness, dyspnea, chest discomfort, occasionally hemoptysis.
-2 major presentations: “Cavitary disease in pts w underlying lung dz who are primarily White, middle-aged men, smokers with underlying copd or in patients in whom MAC develops in areas of prior bronchiectasis. Nodular/bronchiectatic disease in patients without previously diagnosed lung disease, including nonsmoking women over age 50 who invariably have bronchiectasis on chest radiography. In retrospect, these patients almost invariably have chronic respiratory symptoms, primarily cough, and recurrent respiratory infections. The presence of bronchiectasis is an important NTM lung disease predisposition regardless of the etiology, such as cystic fibrosis and pulmonary ciliary dyskinesia.”
-DX requires bronch + biopsy. Diagnosis of nontuberculous mycobacterial infections of the lungs - UpToDate
-TX: Antimycobacterial tx is prolonged and potentially difficult to tolerate and should only be considered in patients who meet the clinical, radiographic, and microbiologic criteria for the diagnosis of NTMs
-Some MACs are resistant to MAC so dont give it.
-Patients with cavitary disease, treatment failure, and macrolide-resistant infection should be evaluated for lung resection.
PTX
-Document site and date of occurrence, What caused it,
-if chest tube—who placed it, what site, output amount and color, leak and plan for removal.
- Daily CXR- document if any residual PT X after chest tube removal
- obtain CXR 4 hours after chest tube removal
-Pts with large air leak, empyema, hemothorax, tensionPTX, barotrauma=Large chest tube 24-28Fr
-Smaller ptx=small bore catheter(pigtail<14Fr) or small chest tube <22Fr
-Chest tube sizes- https://www.uptodate.com/contents/thoracostomy-tubes-and-catheters-placement-techniques-and-complications?search=chest%20tube%20size&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1
PE
-Supplemental O2 for goal SaO2 >90%
-see PERT pdf in ‘for work’ folder
-Well’s criteria for dx probability(>6 is high , 2-6 is mod sPESI >1 means higher mortality and tx in patient, bleeding criteria and thrombolytics contraindications in ‘for work’ folder
-Severe hypoxemia, HD collapse, or resp failure=consider intubation
-If intubating GET EXPERT in cardiovascular anaesthesia
-If HD unstable can do cautious IVF 50050-1L NS vs large volumes,
-Initiate pressor if IVF fails
-if HD stable, low risk of bleeding, high suspicion PE= empiric AC even if no CT yet
-if HD stable, if absolute contraindications/high risk of bleeding= NO AC
-if HD stable, moderate risk of bleeding= case by case for AC
-if HD UNSTABLE, high high suspicion of PE=systemic thrombolytic rather than empiric AC
-Hold AC if giving thrombolytics then resume after
-if thrombolytics fail or contraindication > surgical or catheter embolectomy, catheter thrombolysis
-if HD UNSTABLE, low/mod suspicion of PE=empiric AC
-AC choices for acute PE= LMWH, fondaperineux, DOACs
-AC with Heparin, can consider PO if stable, can consider NOACs
-Thrombolytic therapy if unstable, despite heparin
-AC for minimum of 3 months
-Can consider Filter if pts at high risk of bleeding or cant do AC(HD stable pts)
-DO NOT use PROPOFOL if concerned about PE
Lung Nodules
- Document site, and win diagnosed, CT findings, history of active or passive cigarette exposure, who manages patient outpatient, follow up plan
Neuromuscular Diseases(ALS, MS, MD, MG, spinal muscular atrophy)
-These patients may end up with tracheostomy. If patient trached document date of trach, type, size, and if 24/7 trach collar or vent at baseline
- these patients usually need higher TV to prevent air hunger
pHTN
-Hypoxia is the most important and potent stimulus of pulm vasoconstriction
-chronic AC/CCBs to lower systemic arterial pressure
-pulm Vasodilators
Group 3 is 2nd most common phtn type. Group 1 is first
ILD ph worse than copd ph
Severity of ph doesnt correlate with severity of lund dz
-ddx of ph...
-enlarged pa trunk 29mm is cut off
-rhc is gold standard
Status Asthmaticus plan
-Monitor AutoPEEP- goal <10cmH2O
-ABG(normal pco2 and acute asthma indicates severe airflow obstruction)
-RR- can drop all the way down to 6
-I:E ratio 1:3, 1:5
-Increase flow rate to 80-100 (60 to 75 L/min per uptodate)
-0-5 of peep
-consider paralytic
-Solumedrol 125mg q6
-Epi 0.3- 0.5 1:1000 IM
-SpO2 goal >92%
-pPlat<30
-Stack nebs if hasn’t received already in ED 10-15mg albuterol in 1hr(patient doesn’t tolerate albuterol due to coughing, you can do epinephrine 0.3-0.5 mg q20 men’s X3 doses)
- Standard nebulization – Albuterol 2.5 to 5 mg q20 minutes for three doses, then 2.5-5 mg q1-4hrs PRN
- SAMA- ipratropium 500 mcg 4-8puffs by MDI, q20mins for three doses, and then PRN for up to 3hrs.
-Can just do DuoNeb
- Magnesium sulfate (2 g infused over 20 min) x1 dose—CI in renal insufficiency
- Hypotension due to dynamic hyperinflation and poor venous return is treated with fluid resuscitation and prompt alleviation of hyperinflation, usually by temporarily disconnecting the ventilator circuit from the endotracheal tube
-Can decrease TV to allow permissive hypercapnia
Management of ACS in Sickle Cell Disease
-ACS=fever and or respiratory symptoms, a new pulmonary infiltrate on cxr. (Maintain high suspicion even in the absence of cxr findings) -causes=pulmonary embolism, fluid overload, opiate narcosis, alveolar hypoventilation(due to pain), infection. -Labs: cxr, cbc, bmp, lfts, typing screen, HbS, blood cultures, sputum cultures, urine strep/legionella, maybe mycoplasma pcr, RVP extended, ABG if SO2 less than 94%, consider ctpe -ensure patients offered pneumococcal vaccination,abx prophylaxis. Pts will be on chronic transfusions at home or could be on hydroxyurea(it helps produce more fetal hemoglobin that way HbS is not too much in body) -can consider BAL for viral/bacterial studies -Tx plan - Consult Transfusion medicine, Heme/onc, consider ID consult - IS is beneficial in patients with chest or rib pain - ABXs and cover for atypicals + consider antivirals -Early PRBC transfusion can be considered but if severe disease need exchange transfusion. -give broncho dilators if clinical features suggestive of a checks of asthma or there's a cute bronchospasm -oxygen for Spo2>94% -IV fluids(individualized based on cardiopulmonary status, avoid pulmonary edema/overload) -pain management-use opiods, ketorolac -Exchange transfusion(usually about 8uprbcs) with post transfusion HBs target <20-30% -Consider ECMO early if patient worsening, developing ARDs -unproven considerations= nitric oxide, corticosteroids(not recommended d/t side effects but can consider use in acute asthmatic),
Myasthenia Crisis Plan
MG crisis is a life-threatening exacerbation of MG characterized by neuromuscular respiratory failure
Causes include spontaneous, infxn, surgery, or tapering of immunotherapy, initiation or tapering of steroids, medications that can increase weakness in myasthenia.
-ICU admit
-Consider ETT if VC < 15-20mL/Kg of body weight, MIP/NIF is less negative than -30cmh2o or resp distress
-d/c anticholinesterase meds(pyridostigmine) to reduce airway secretions. can restart at lower dose.
-Rapid immunotherapy (plasma exchange > IVIG
-Concurrent initiation of chronic immunomodulating therapy(prednisone, azathioprine, mycophenylate, efgartigimod alfa, ravulizumab, cyclosporine, or tacrolimus
Carbon Monoxide (CO) Poisoning
-Risk factors: smoke inhalation, fuel-burning heaters
-Sx: headache, nausea, and dizziness
-PE: altered mental status, cherry-red skin (postmortem finding)
-Pulse oximetry does not distinguish between carboxyhemoglobin and oxyhemoglobin
-Labs: ABG - carboxyhemoglobin
-Treatment is 100% oxygen, hyperbaric oxygen in some high risk patients (ex coma, pregnancy)
Anaphylaxis plan
-Pepcid
-Benadryl
-Dexamethasone
-Epi
OD plan
-note time of ingestion
-serial EKGs to monitor changes
Aspergillosis
-A. fumigatus is MCC of human disease
-risk factors: immunocompromised, neutropenia, chronic granulomatous disease,
-aspergillus affects innate immunity(neutrophils) so not commonly seen in HIV pts
-Invasive aspergillosis- occurs in most immunocompromised pts, with neutrophil dysfunction, primary pulmonary infenction, early CT scan will show small multiplel ung nodules
-obtain Bcx, rcx, BD glucan and galactomannan in blood and BAL
-Tx: reduce immunosuppression(increase neutrophils), Azoles(vori, posa, itra, amph B, micafungin
ILD
-can be grouped as exposure related ILDs(hypersensitive pneumonitis, pneumoconioses, radiation, medication induced)
Connective tissue related ILDS(SS, RA, polymyositis, dermatomyositis, lupus) or
Idiopathic ILDs(IPF, NSIP, organizing pan, AIP, bronchiolitis ILD) or
other ILDs(sarcoidosis, vasculitis, eosinophilic pan, pulmonary langerhans cell histiocytosis)
-sx= chronic or progressive dyspnea, nonproductive cough, hypoxemia, fine crackles,
-Tx options include supportive, O2, steroids
Cardiac System
Cardiogenic Shock
See hypotension section in DDX by Vital Signs
1. Is definition criteria met?
Shock= hypotension (SBP<90mmHg, MAP<60mmHg)+ lack of end organ perfusion(low UOP, AKI, shock liver, AMS, stroke, MI, blue fingers/toes)
2. Determine Primary insult and compesatory mechanisms
2.1. Exam findings
--cold distal extremities(check calf. this means low CO or high SVR)
--wet/hypervolemic(sob, crackles, orthopnea, ascites, pitting edema), elevated JVD
--Hx(of MI, HF, or valvular dZ)
--echo with low EF, IVC>2cm in size wo resp variation
--elevated LA, low ScVo2 <65%, SVo2 <50%
--echo and venous sat are best to confirm diagnosis of cardiogenic shock
3. Treat
Goals are to
-increase co (inotropes(dobut/milrinone))
-Decrease SVR (vasodilators like nitroprusside)
-decrease CVP (diurestics)
-Consider mechanical support i.e Impella, ballon
-Dobutamine causes less hypotension and arrythmia than milrinone.
-Milrone is a more potent vasodilator so can cause hypotension
-nitroprusside can cause cynanide toxicity
MAP=CO x SVR
SVR=[(MAP-CVP)/CO] x 80
CO= SV x HR
Stroke volume=preload, afterload, contractility
Heart Failure
-Causes: CAD, HTN, pHTN, Cardiomyopathy, arrythmia,
-compesatory physiologic mechanisms: enlargement, increased muscle(hypertrophy), tachycardia, increased systemic SVR to try to increase blood flow.
-Can be acute or chronic
Acute RV failure
-Avoid volume overload
Don’t give more fluids!!
Be judicious if needed
-Avoid systemic hypotension
Use Norepi, epi early
Avoid phenylephrine as it’s pure alpha and constricts systemic + pulm vessels
Vasopressin spares pulm vessels
Consider inotropes (dobutamine/milrinone) though both can cause hypotension
-Manage RV afterload
Hypoxia increases afterload so liberalize O2
Keep vasodilator infusions going
Consider vasodilator
-Avoid intubation
-Get A line
AV Blocks
-Differentiate Mobitz 1 vs 2 by looking at PR interval, if just 1 is changed, its type 1.
-Advanced AV block or high grade av block= AV block with > 3:1 conduction
-Mobitz II is infranodal so QRS will always be prolonged
-Mobitz II does not respond to Atropine, neither will be pressors
-Transcutaneous pacing and TV pacing if worsens
-Permanent pacer when able
Atrial Fibrillation/ Afib
-Preferred to use Rate vs rhythm control
-Types: paroxysmal, persistent, longstanding persistent, or permanent AR
- If conversion to SR (either spontaneous or via cardioversion) occurs within 48 hours of the onset of AF, the thromboembolic risk appears to be very low
- For most patients in whom cardioversion will take place less than 48 hours after the onset of AF, we start a DOAC prior to cardioversion rather than no anticoagulant. Intravenous heparin is a reasonable alternative for hospitalized patients.
- For patients at very high bleeding risk, some of our experts suggest cardioversion without anticoagulation if normal SR can be restored within 48 hours of documented onset. Other experts recommend anticoagulation prior to cardioversion even in these high-bleeding-risk patients.
- If cardioversion needs to take place within three hours, whether for patient instability or convenience, start intravenous unfractionated heparin.
-When in need of urgent cardioversion for afib refractory to chemical agents, consider bolus of heparin. Prior to cardioverting. Consider AC 4wks post cardioversion unless contraindication.
RP bleed plan
1. Stop heparin/anticoagulation
2. Obtain CTA after considering scr/gfr
3. Call vascIR , gen surg if pushback
4. Send type n screen.
5. Call hcp, obtain transfusion/aline/cline consent.
NSTEMI plan (even if not cathed)
- heparin drip.
- Continue ASA 81 milligrams PO daily.
- High dose statin daily.
- Consider Brilinta versus Plavix. Post cath. Send PA
- Consider ACEi/ARB/entresto daily if reduced EF. Just diuresis if hfpef
- Trend Troponin to peak
-A1c/Lipid panel
-Consider BBlocker initiation (don’t give if HF)
-NPO @midnight for cath
NSTEMI UpToDate Tx:
- 162 to 325 mg of asa ASAP after diagnosis being made.
-p2y12 inhibitor in all patients(can do load)
-Glycoprotein 2b/3a inhibitor in select patients
-give PPI in pts with a history of or at high risk for GI bleeding.
-Bblocker in all acs. Except if signs of hf. Metop succinate.
-anticoagulantionl in all ACS patients to reduce risk of intracranial and catheter thrombus formation.
Long-term mmgt post ACS
-ASA forever, DAPT* 12 months (no need for dapt if cabg?)
-bblocker unless contraindication (use metoprolol, atenolol, carvedilol, or bisoprolol)
-ace inhib (appropriate in htn, ckd, dm, or EF less than 40%)
-ARB if already on bb, Ace and have EF less than 40%.
-artovastatin 40 to 80 daily or rosuva 40 mg daily
-for pain use apap or tramadol, avoid nsaids.
Hemorrhagic shock plan
-Avoid delay in definitive tx: page GI/IR and or Surgery or OB
-1:1:1 transfusion ration in trauma pts
-1:2 ffp:prbcs in nontrauma pts
-Can do TXA 1g within 10mins then 1g OVER 8hrs
-can add vasopressor if needed
-Minimize crystalloid- excessive ivf associated with worse outcomes, dilutes clotting factors
-obtain CBc, t&c, coags, fibrinogen, LA, ABG, TEG, markers of organ injury
-monitor for signs of transfusion risks: infection, fever, volume overload, TRALI, transfusion reaction, citrate toxicity, hyperkalemia, hypocalcemia, hypothermia.
-Reverse anticoagulant
-consider DDAVP if plt dysfunction
Abdominal Aneurysm plan
-control HR<60, BP<170
-avoid narcotics
-consult vascular surgery
-ASA daily?
-Esmolol gtt for HR/BP
Digestive/Gastrointestinal System
HTG-induced pancreatitis (HTGP)
Causes: Primary(genetic/familial hypertriglyceridemia, 2ndry (DM, Alcohol, medications, pregnancy)
-Plasmapharesis if pt with worrisome features(hypoCa, LA, and worsening SIRS by Modified Marshall scoring system)
-Insulin- 4pts w/ worrisome features and plasmapharesis is indicated but unavailable/cannot be tolerated
-Pts wo worrisome features, no hyperglycemia, evidence to support the use of insulin is lacking
-regular insulin gtt 0.1 to 0.3 units/kg/hour - stop when TG <500
-Fluid replacement- can do LR 200cc/hr-x24-48hrs- timing, rate, type of fluid, duration of tx unclear,so don’t overload
-Pain control- dPCA or fentanyl, Meperidine >morphine
-Nutritional support- fat restriction, restart po feeds within 24hrs if pt can tolerate and no ileus signs
-check CBC for hemoconcetration d/t fluid loss
-Check TGq12
-Consider Endocrine consult
-give more fluid if hemoconcetrated
-Will need longterm lipid management with Gemfibrozil, fat restriction, weight loss
Acute Pancreatitis
Causes: Gallstones, alcohol, ERCP, genetic, HTG, meds, pancreatic duct injury, rare(biliary sludge, biliary obstruction, hypocalcemia, infections, vascular dz)
-Fluid replacement- can do LR 200cc/hr-x24-48hrs- timing, rate, type of fluid, duration of tx unclear,so don’t overload
-Pain control- dPCA or fentanyl, Meperidine >morphine
-Nutritional support- fat restriction, restart po feeds within 24hrs if pt can tolerate and no ileus signs
-check CBC for hemoconcetration d/t fluid loss
-give more fluid if hemoconcetrated
Acute Pancreatitis
-Presents with abdominal pain, radiating to the back
-ddxs include:
-causes: gallstones>alcohol, hypertriglyceridemia, hypercalcemia, drugs, scorpion bites
-IVF isotonic crystalloid fluids @ 5-10ml/kg. LR contraindicate if d/t hypercalcemia
-PAin management with opioids
-Nutrition, can restart slowly, make NPO initially
-PLEX (plasma pharesis) if d/t hypertriglyceridemia. Consult Transfusion MEdicine
-Continuous insulin gtt if d/t high TGs. Give d5NS/LR as glucose source
-ABXs only if suspected infection
-Complications: ACS, ARDS, effusions, MI, AKI, Ascites, DIC, hypocalcemia, necrotizing pancreatitis, pancreatic pseudocyst,
UGIB
-Presented with hematomises and or melena. Ddxs include PUD (secondary to h pylori, nsaids), esophagitis/duodenitis, vascular lesion(angiodysplasia, dieulafoy lesion), bleeding varices, duodenal/gastric ulcer, mallory weiss tear, tumor
- -Maintain Large bore pIVs
-if HD unstable / severe bleeding>resuscitate with blood products, emergent EGD
-Consult Surgery/IR if endoscopy unsuccessful or cannot be performed.
-Consider colonoscopy if no source identified
-if still no source and severe bleeding present, obtain CTA, if no source consider small bowel enteroscopy, Merckel scan, Tagged RBC scan, laparoscopy / laparotomy with enteroscopy.
- Avoid NSAIDs
-Hold Anticoagulants/antiplatelets
-PPI IV bolus then BID
-if Hx of cirrhosis, give prophylactic ABX with CTX.
-Consider reversal of coagulopathy if present
-if variceal bleeding suspected, start octreotide drip with bolus
-Consider balloon tamponade
-Consider evaluation for Tips
-if HD stable, EGD within 24 hours
If EGD no source, plan for colonoscopy, if that is negative, evaluate for small bowel bleeding.
LGIB
-Presented with hematochezia, can be melena. Ddx's include diverticulosis, angiodysplasia, colitis, IBD, colon cancer, anorectal disorder, hemorrhoids, radiation induced injury.
-GI consult
-Consider IR consult/Surgery consult
-Consider reversal of coagulopathy if present
-NPO
-Maintain Large bore pIVs
-if HD unstable, resuscitate, consult surgery/ir, EGD once HD stable, if no source and bleeding continues then CTA, if bleeding not severe do colonoscopy.
-if HD stable, plan for colonoscopy
-bowl prep with go lytely
-NO NEED for PPI
Tagged rbc is most sensitive for lower gi bleed.
Jehovah Witness GIB
-Ask about history of peptic ulcers, gastritis, that particulosis, polyps, IBD, hemorrhoids, of a disease, alcohol use, recent trauma / injury, vomiting.
-ask about source, onset, and duration of bleeding, color, and volume, use of ACs or asa/nsaids.
-s/s jaundice, ascites, hepatic disease signs, purp lesions, petechiae, moses, telangictasia's, splenomegaly
-ddxs(pud, esophageal varices, z e s syndrome, esophagitis erosive, AVM, intestinal polypopsis, previous GI surgery
-Consider stopping drugs or drug interactions that may adversely affect hemostasis including steroids, ssris, abxs
-send cbc, INR, BMP, I
Lfts, hpylori
-get egd within 12hrs of admission
-consider colonoscopy
-consider early angiography/embolization
-consider vce
-empiric high dose ppi,h2ra, antacid + octreotide gtt
-urhent surgical evaluation if above measures unable to stop bleeding
-give crystalloids judiciously, consider colloids
-tolerate mild-mod hypotension(90-100) until bleeding controlled.
-hemostasis agents(ddavo, vit k, novoseven/factor7a, erythropoeitein/procrit, TXA
-Restrict phlebotomy, perform only essential tests
Autoimmune hepatitis
- obtain serum AB checks, ana, othe rheumatological labs
-intial tx with prednisone +- azithiophrine
Cirrhosis
-Consider SBP ppx, Ulcer ppx
-Obtain Child Pugh class (measures severity of liver disease)
-Obtain maddrey score (estimates disease severity and mortality risk in pts with ALCOHOLIC hepatitis)
-Daily MELD (predicts 3month survival, helps to prioritize pts waiting for transplant)
-Consider workup for Liver transplant
Nutrition consult
Cirrhosis Complications
Variceal bleeding:
-pt will present with hematemesis or melena
-EGD ideally within 12 hrs of presentation
- esophageal varicces= band ligation preferred over sclerotherapy-can give erythro/reglan prior to procedure
-gastric varices-injection of tissue adhesive cyanoacrylate vs TIPS
-Ectopic varices-TIPS vs surgery, endoscopy tx often unsuccesful
-if rebleeding consider repeat egd tx before tips or surgery.
-transfuse for Hgb<7 for goal 7-9, PLTS <50K,
-CTX 1g q24hr x7days for ppx
-Octreotide or vasopressin x3-5days or per GI
-resume enteral nutrition 48-72 hrs post last esophageal bleed
-Consider Blakemore tube insertion
-Consider TIPS if rebleeding--For patients with actively bleeding esophageal varices who either fail first-line methods of hemostasis or who have initial hemostasis but then rebleed within five days, TIPS is an option for achieving both short- and long-term hemostasis.
Portal hypertensive gastropathy:
-Consider TIPS
Ascites:
- Baclofen can be given to reduce alcohol craving and alcohol consumption in patients with ascites in the setting of alcoholic liver disease
- Firstline treatment of patients with cirrhosis and ascites consists of sodium restriction (88 mmol/day [2000 mg/day]) and diuretics (oral spironolactone with or without oral furosemide).
- Fluid restriction is not necessary unless serum sodium is less than 125 mmol/L.
- An initial therapeutic abdominal paracentesis should be performed in patients with tense ascites.
-Sodium restriction and oral diuretics should then be initiated.
- Liver transplantation should be considered in patients with cirrhosis and ascites.
-Avoid NSAIDS/ACEis/ARBs
-Consider TIPS if refractory to diuretics
Spontaneous bacterial peritonitis:
- Start empiric antibiotics if temp> 37.8, Abd tenderness, AMS, PMN count>250cells/microL
- cefotaxime 2 g intravenously every eight hours x5-10days preferred but can-do 3rd Csporin
- If CTX is used, dose is 2g per day.
- Discontinue nonselective beta blockers.
- Consider albumin administration in patients with renal dysfunction
-consider Repeat paracentesis/PMN count to monitor for improvement
Hepatorenal syndrome:
-DX is chronic or acute hepatic dz with advanced hepatic failure/pHTN + AKI (KDIGO criteria)
-/is pt Liver transplant candidate? If no, consider need for ICU.
-Levophed gtt to raise MAP by 10mmHg, consider adding vasopressin
-Albumin 1g/kg (100g/day max) x 2days
-Consider midodrine, Octreotide gtt 50mcg/hr or 100-200mcg TID SQ x2wks
-Consider TIPS
-Consider RRT(HD)- dialysis as a bridge to liver transplantation or liver recovery.
Hepatic Encephalopathy:
-Look for precipitating cause(GI bleed, renal failure, hypo/oxia/glycemia/kalemia, constipation)
-Lower ammonia: Lactulose + Rifaximin
Portal Vein Thrombosis (acute):
-Anticoagulation- need to screen for varices prior to AC initiation
-use LMWH then can transition to warfarin or DOAC x3-6months
Large Bowel Obstruction
-DDXs include toxic megacolon, mechanical obstruction, chronic intestinal pseudo-obstruction.
-Cecum usually most dilated
-small bowel won’t be dilated unless severe obstruction with ileocecal junction dysfunction
-Do not give PO barium
Acute colonic pseudo-– obstruction(Ogilvie’s syndrome)
-NGT to suction
-Insert malencoat rectal tube
-NPO
-CT a/p STAT
-Surgery consult STAT
-Consider GI consult-can do colonoscopy to decompress
-check CBC,BMP, Mg, LA, BID
-Serial Abd exams
-KUB q12-24
-consider barium enema
-Neostigmine 2mg x1 if indicated in patients with acute colonic pseudo-obstruction and cecal diameter >12 cm or in patients who fail 48 to 72 hours of conservative therapy.
-supportive management 48-72hrs if no significant abdominal pain, colonic distension>12cm, peritonitis
-discontinue bowel regimen, avoid laxatives
-avoid opioids, anti-cholinergics, calcium channel blocker's.
- If successful colonic decompression, administer polyethylene glycol electrolyte balanced solution to decrease the risk of recurrence [26,37].
-Patients with a partial response or recurrence after initial resolution should be treated with repeat administration of neostigmine [36]. It is the author's practice not to repeat dosing within 24 hours.
- ASGE guidelines- https://www.asge.org/docs/default-source/education/practice_guidelines/doc-the-role-of-endoscopy-in-the-management-of-patients-with-known-and-suspected-colonic-obstruction-and-pseudo-obstruction.pdf?sfvrsn=b9fc4951_6
(Volvulus—closed loop bowel causing Large bowel obstruction
-small bowell wil be dilated
-high risk of strangulation
-can use colonoscopy to reduce/
Stercoral Colitis
-a rare inflammatory form of colitis that occurs when impacted fecal material leads to distention of the colon and eventually fecaloma formation. Fecalomas can lead to focal pressure necrosis and perforation, while colonic distention and increased intraluminal pressure can lead to compromise of the vascular supply and ischemic colitis.
-etiology: chronic constipation, colonic distension. Risk factors include(for developing chronic constipation are multifactorial and include low fiber diet, genetic factors, behavioral factors, pharmaceutical factors)
-DDX: diverticulitis. Largel bowel obstruction, infectious colitis, malignancy, bowel perf, acute mesenteric ischemia, intra abd abscess.
-Exam findings: for developing chronic constipation are multifactorial and include low fiber diet, genetic factors, behavioral factors, pharmaceutical factors, septic shock presentation
-Labs: Elevated lactic acid and anion gap metabolic acidosis in the setting of stercoral colitis should raise concern for bowel ischemia or perforation.
-Obtain Bcx, coags,
-Obtain CTAP with IV contrast if renal fxn allows
-Tx: if no signs of peritonitis then can manage nonoperatively: manual disimpaction, bowel reg, NPO. Pain mgnt with nonopiods, pts with septic shock(give IVF, BSABXs with anerobic g- coverage).
- Operative management is reserved for patients with perforation, patients who have large segments of bowel involvement, or if conservative management fails. Treatment for these patients involves resection of the affected bowel, colostomy, and Hartmann pouch
- Osmotic and stimulant laxatives are considered first-line treatment for patients with constipation.
Genitourinary system
AKI: See ddx by symptom section: Oliguria/Anuria sectionRhabdomyolysis plan
Causes:hyperthermia, trauma, compartment syndrome, strenous muscle activity(SZR, asthmaae, agitation, NMS/SS), inflammatory myopathy(dermatomyositis, immune-mediated necrotizing myopathy, antisynthetase syndrome, polymyositis) medications(statins, colchicine, antidepressants/antipsychotics, antimicrobials, propofol, interferon, sympathomimetics), electrolyte abnormalities, infections especially viral
-start isotonic bicarb (150 meq/l) at a rate of 150-200mL/hr to help augment your output for a goal of 200 mL per hour.
-Renally meds for GFR<10
-avoid nephrotoxic agents
-foley catheter for accurate I/Os
-will likely have hyperphosphatemia due to rhabdomyolysis causing intercellular phos release
-Monitor K as rhabdomyolisis can cause hyperkalemia
-The serum CK begins to rise within 2 to 12 hours following the onset of muscle injury and reaches its maximum within 24 to 72 hours.
-A decline is usually seen within three to five days of cessation of muscle injury.
-CK has a serum half-life of approximately 1.5 days and declines at a relatively constant rate of approximately 40 to 50 percent of the previous day's value
-CK not elevated in hemolysis
HyperKalemia management
-symptoms include muscle weakness, ventricular arryhthmias. Causes include increased k release d/t (severe hyperglycemia, rhabdomyolysis) or decreased secretion 2/2 to (hypoaldasteronism, renal failure)
- D50W of glucose
-10U Reg Insulin IV
-calcium gluconate 1000 mg (10 mL of 10% solution) or calcium chloride 500 to 1000 mg IV over two to three minutes.
-KAyaxxalate post code or emergent period
-RRT should be planned for ESRD pts
-Diuretics for pts making urine(can do Lasix 40mg can do single dose up to 80mg per umass protocol
-Consider insulin gtt with dextrose source if cant get hd
-Can use bicarb (use drip instead of amps)
Tumor Lysis Syndrome
-rasbuticase for uric acid >8, phos binder for >4.5
Endocrine system
DI plan
-An increased amount of tasteless urine as opposed to sweet(mellitus).
-Causes: can be nephrogenic (kidneys don't respond to ADH), Gestational(vasopressinase), Dipsogenic (drinking lots of water), Central/AVP-D(ADH not being released or produced)
-Tx for Central/Gestational DI= Desmopressin, see below
-Tx for nephrogenic=thiazide diuretics(increases urine excretion of sodium)
-Tx for dipsogenic=stop drinking so much
-Central DI plan:
-BMP, serum Osm, urine osm, UA(specific gravity) q4h
-HOB>45 degrees at all times
-Bowel regimen to prevent straining
-DDAVP if UOP > 250cc x3hrs consectively
Pt can drink to thirst
-Nasal precautions (post transphenoid surgery): nothing up the nose, no NC, no nasal swabs, no nose blowing, sneeze with mouth open
Myexedema Coma
-In myexedema, give steroids first before replacement thyroid
Thyroid Storm
Hematology/Oncology Systems
Neutropenic Fever
- Definition=Fever in neutropenic patients is defined as a single oral temperature of >38.3°C (101°F) or a temperature of >38.0°C (100.4°F) sustained for >1 hour. (ANC) <500 cells/microL or an ANC that is expected to decrease to <500 cells/microL over the next 48 hours.
-Often only evidence of infection is bacteremia
-MC bugs are GPCs. GNBs usually mean worse infection. Candida and aspergillosis are MCC fungal infxns and are common in high risk pts
-Tx=early ABXS
Multiple myeloma
-CRAB(hypercalcemia, I know failure, anemia, bone pain)
-serum Labs include esr, CBC with peripheral smear(roleux formation) CMP, uric acid, Spep, immunofixation,serum alp, b2 microglobulin, plasma immunoglobin level / plasma protein level.
- urine labs=upep/immunofixation, urine lytes
- imaging= cxr, mri
-bone marrow biopsy is definitive.
Tx
-immunomodulator(lenalidomide, thalidomide), proteosome inhibitor(bortezomib), steroids(dexamethasone)
-autologous stem cell transplant in younger patients
- consider palliative care in elderly (cyclophosphomide-alkylating)
-radiation can be considered
-CYBORD
HITT
-score is 6-7, then have to send SRA(takes 5 days to result)
-Obtain HIT antibody, comes back quicker
-Have to anticoagulate with Argatropan
SIckle Cell disease/management of Acute chest syndrome in SCD
-An acute illness characterized by fever and or respiratory symptoms accompanied by a new pulmonary infiltrate on CXR. severe hypoxia is a useful predictor of outcome and severity.
--Etiology/trigger: pulmonary infection(chlamidia/RSV in adults, mycoplasma in children), fat embolism, asthma, PE, fluid overload, opiate narcosis, hypoventilation,
-Presentation: may present in ACS or before so have to be vigilant with these pts. Can present as hypoxia without cxr findings.
-Worsening hypoxia, increasing RR, decreasing PLTs, Hgb, multi lobar cxr involvement or neurological findings all equals bad news
-Workup: CXR, full CBC, T&S/c, CMP, Bcx, Sputcx, RVP, mycoplasma, ABG, CTPE, check smear for red cell agglutination/cold agglutinnins
-Give ppv pneumovax vaccine, Hif tybe b, meningitis vaccine
-Consider RHC for cor pulmonale?
-TX: opiods, IS, ABXs(cover atypicals), antivirals if h1n1 suspected
-Exchange transfusion to target lower HBs level
-Nebs if asthma present
-IV fluids but don’t overload
-daily CXR essential
-Heme consult