Leukostasis

Thanks to Grace for presenting the case of a middle aged man who presented with chronic weight loss, acute SOB, and splenomegaly on exam, found to have a WBC of 188 on work up and chest imaging concerning for leukostasis.


Clinical Pearls

  • Most common cause of splenomegaly is portal HTN.  But the ddx is broad (see schema below).
  • Most common cause of a WBC 25k-75k is infection (C diff)
  • WBC >100k is leukemia until proven otherwise.
  • Leukostasis is symptomatic hyperleukocytosis, most commonly associated with AML.
  • Management involves lowering the WBC by leukapharesis, hydrea, and TKIs (if CML) and preventing TLS.

Splenomegaly DDx

  • ↑ Water: portal HTN (most common cause)
  • ↑ Cells:
    • RBCs
      • Hemolysis ⇒ Thalassemias, hereditary spherocytosis, malaria, babesia
    • WBCs
      • Infection
        • Mono ⇒ EBV, CMV, HIV
        • Tick-borne ⇒ Rickettsia, anaplasmosis, ehrlichiosis
        • Granuloma ⇒ TB, histo, leishmaniasis
      • Autoimmune
        • Sarcoid
        • Still’s
        • Felty
      • Lymphoma
      • Myeloproliferative d/o
        • Polycythemia vera
        • Essential thrombocythemia
        • CML
  • ↑ Molecules:
    • Amyloidosis
    • Other (lysosomal and glycogen storage diseases)

Leukostasis:

  • Defined as symptomatic hyperleukocytosis and is a hematologic emergency!
  • Mortality rate can be as high as 40% within the first week of presentation.
  • Clinical manifestations of ischemia primarily in CNS, MI, lungs, and kidneys.  Can also see limb ischemia and priapism.
  • Malignancies at highest risk of leukostasis in order of prevalence:
    • AML (WBC >50k)
    • ALL (WBC >100k, though tends to present with TLS and DIC much more commonly than leukostasis)
    • CML (WBC >100k), generally if in myeloid blast crisis
    • CLL (WBC >400k)
  • Treatment:
    • FLUIDS, lots and lots of fluids
    • Cytoreduction: lowers the WBC
      • Leukapharesis: not readily available as it requires a dialysis line and trained nursing staff
      • Hydroxyurea: to lower the WBC
      • Tyrosine kinase inhibitors (especially for CML related leukostasis)
      • Induction chemo (for non-CML related leukostasis)
    • Prevent tumor lysis syndrome:
      • FLUIDS
      • Allopurinol
      • Uric acid lowering therapy
    • In hemodynamically stable patients AVOID TRANSFUSION – it’s like adding fuel to the fire and can worsen ischemia. Platelet transfusion is less dangerous than RBCs and you may have to do it before trialysis line placement.

TLS:

  • ↑K, ↑Phos, ↑uric acid, ↑creatinine, ↓calcium
  • Occurs in bulky or chemosensitive tumors with high proliferative rate (Burkitt’s lymphoma, acute leukemias, small cell lung cancer)
  • Allopurinol takes 1-2 days to show effect and does not reduce preexisting elevated uric acid levels so use rasburicase if uric acid already high or preemptively if TLS risk is high or if there is kidney injury.
  • HD if concern for renal damage

Causes of pseudohyperkalemia

  • Technique of blood drawing (tourniquets and fist pumping)
  • Thrombocytosis
  • Leukocytosis (>120k)

 

 

ECG Report #2!

Thanks everyone for yet another high yield report on ECGs with Dr. Zhao!  Here are the main pearls from today:

  • Remember that a negative p wave amplitude in lead I is seen in two diagnoses only: dextrocardia and limb lead reversal.  To distinguish between the two, look at the amplitude of the QRS complexes as you advance through the precordial leads.  In dextrocardia, you should see a loss of amplitude as you go from V1 to V6, because you are getting further away from the heart.  In limb lead reversal, this is not the case.
  • Remember that ST depressions in anterior leads V2 and V3 should raise your suspicion for a posterior MI and prompt further evaluation with a posterior ECG!
  • When dealing with an irregularly irregular wide complex tachycardia, think of these three differential diagnoses:
    • Atrial fibrillation with aberrancy (i.e. with a bundle branch block)
      • QRS waves should largely look similar in morphology
      • Rates should not exceed 170 bpm because all conduction is still going down the AV node
      • Treatment: shock if unstable, AV nodal blocking agents or amiodarone
    • Atrial fibrillation with an accessory pathway (WPW, also known as a preexcitation pathway)
      • QRS waves have varying shapes because they are conducted down the accessory pathway and the AV node
      • Because the accessory pathway has a much shorter refractory period than the AV node, heart rate can be very high and >200 bpm.
      • Treatment: shock if unstable.  Do NOT give AV nodal blocking agents (including amiodarone) because blocking the AV node can force all conduction down the much faster accessory pathway and lead to VF arrest.  The agent of choice is IV procainamide.
    • Polymorphic VT
      • QRS morphology varies (Torsades)
      • Rates should not exceed 170 bpm
      • Treatment: shock if unstable, otherwise amiodarone

ANCA-mediated glomerulonephritis! 03/14/2019

Happy Pi Day!

Thanks to Brayden for presenting a case of a 48yo M with no significant medical or family history presenting with 2-3 months of LE edema, generalized weakness, malaise, myalgias, and arthralgias (general, no particular pattern). He was found to be anemic, and urine studies were notable for nephritic range proteinuria and microscopic hematuria. His complements levels were normal. Ultimately renal biopsy revealed the presence of crescents in the glomeruli, and MPO positivity indicating a P-ANCA related vasculitides. Based on his history, his final diagnosis is RPGN Type 3 secondary to most likely MPA.


Hematuria: First step is to see if there is actually RBC in the urine! 

  • With RBC
    • RBC Casts, proteinuria, AKI
      • Glomerular pathology
    • No casts, no AKI
      • Non-glomerular bleed
        • UTI
        • BPH
        • Renal cysts
        • Sickle Cell
        • Interstitial disease
        • Nephrolithiasis
        • Post exercise
        • Tumors
    • Without RBC
      • Porphyria, Beeturia, Rhabdomyolysis

All About Casts! Presence of certain casts in the urine can provide useful information.

  • Hyaline casts: Nephrotic syndrome, pre-renal azotemia, normal
  • Fatty oval bodies: Nephrotic syndrome
  • RBC casts: GN
  • Granular cast: ATN, interstitial nephritis, note that you can see ATN even without casts!
  • WBC cast: Interstitial nephritis, acute pyelonephritis, acute GN

Glomerulonephritis

  • Presentation
    • Glomerular inflammatory leading to hematuria, variable range proteinuria, HTN, edema, RBC casts or dysmorphic RBC
  • Etiology
    • Immune Complex Deposition GN
      • Typically LOW complement levels
      • Differential
        • SLE GN: ANA, DS-DNA
          • C3 way lower than C4
        • PIGN (post-infectious or strep GN, infection related GN): Streptococcal antibodies i.e. ASO, recent infection
          • Low C3, Low CH50, normal C4
          • Supportive care + antibiotics
          • Typically weeks after an infection but can occur during infection
        • IgA nephropathy: MOST COMMON, recent respiratory or GI infection, kidney biopsy with IgA deposits, normal complements
        • Cryglobulinemic GN: Cryoglobulin, HCV association
          • C4 way lower than C3
        • Membranoproliferative GN (MPGN): Complement activation, immune-staining positivity on biopsy
        • HSP (nrl complements), palpable purpura, abd pain. IgA, IgG, C3 deposition. Closely related to IgA Nephropathy but with systemic/extra-renal involvement.
        • Subacute bacterial endocarditis (Low C3, fever, + cultures)
        • Atheroembolism: + eosinophilia + eosinouria
    • Anti-GBM (Good Pastures) GN
      • NORMAL complement levels
      • Positive anti-GBM
      • Lung and renal involvement, young patients <30 are more likely to have involvement of both and older patients > 50 are more likely to present with isolated GN. Male predominance in younger patients and female predominance in older patients.
    • ANCA related GN aka Pauci-immune GN (PIGN)
      • NORMAL complement levels
      • Absent extra-renal disease: ANCA-associated crescentric GN
      • Systemic necrotizing vasculitis, P-ANCA/MPO: Microscopic polyangiitis (MPA)
      • Respiratory sx, sinusitis, granulomas, C-ANCA/PR3: Granulomatosis with polyangiitis (GPA)
      • Asthma and eosinophilia, P-ANCA/MPO: EGPA
      • Biopsy: None to few immune deposits in the glomeruli in IF and EM. 96% will be positive for ANCA, the other 4% are ANCA-negative pauci-immune GN
        • Focal necrotizing, crescentic glomeruli
    • RPGN: Rapid renal failure with extensive crescent formation that can lead to ESRD within weeks to months. Can present in any age group.
      • Association: Goodpasture, SLE, GPA, idiopathic
      • Complements: Nrl
      • Bx: Crescent formation in > 50-75% of glomeruli
      • IM: Linear IgG
      • Types: 3 types depending on immunofluorescence pattern.
        • Type 1: 20%, anti-GBM
        • Type 2: 25%, immune complex deposition, SLE, GSP, IgA nephropathy, acute proliferative GN
        • Type 3: Aka Pauci-immune GN, 55%, glomeruli damaged in unclear mechanism. Can be idiopathic or related to ANCA associated vasculitis like GPA, MPA, EPGA. Most common.
  • Diagnosis
    • Kidney biopsy for definitive diagnosis but it can be deferred if a diagnosis can be determined via serologies or if pts have fibrotic kidneys, which makes the risks for that diagnostic piece of information outweigh the benefits.
  • Management of GN:
    •  Treat underlying cause if any.
    • Immunosuppression: Usually high dose steroids + cyclophosphamide, rituximab may also be used. Plasmapheresis is also an option.
    • Initial therapy: Methyprednisolone 500-1000mg daily for 3 days
    • No different between use of rituxuimab vs cyclophosphamide (RAVE, RITUXVAS)
    • Cyclophosphamide: Available in PO formulation in a daily dosing, favored by some Nephrologist.
    • Prognosis
      • If left untreated, RPGN progresses to ESRD over weeks to months. Fewer crescents (<50%) is associated with slower progression.

Summary (souce: Grepmed)

GN

FUO for 2 months that turned out to be DLBCL and Cryptococcal pneumonia! 3/13/2019

We worked through a case from the Human Diagnosis Project with a 57 yo M originally form Guatemala (moved to US 25 years ago) with a history of pre-DM and recently diagnosed and treated Lyme disease presenting with 2 months of persistent fever, chills, malaise, and myalgias. He received extensive work up, and everything turned (including TEE, LP, SPEP, rheum, BM biopsy, HIV) were negative. He had splenomegaly on exam, and CT CAP revealed hilar LAD + LLL tree-in-bud along iwth a 20cm spleen. The patient was ultimately diagnosed with DLBCL, AND cryptococcal pneumonia secondary to immunosuppression from his lymphoma!

Credit: Dr. Ron Cho, New York Medical College, Internal Medicine.


Fever of Unknown Origin

  • Classic Definition
    • Fever > 38.3 °C on multiple occasions
    • Duration > 3 weeks
    • Uncertain diagnosis after 3 outpatient visits or 3 days in the hospital (revised, used to be 1 week inpatient investigation) or 1 week of “intelligent and invasive” ambulatory investigation
  • Etiology
    • Infectious
      • TB is the single most common infection in most FUO series, can be extrapulmonary, military, or pulmonary. May occur concurrent in AIDS patient, leading to a more subtle presentation.
      • Abscess
      • Osteomyelitis
      • Bacterial endocarditis (2-5% of these are culture negative bacterial endocarditis, i.e. from Coxiella brunetii and tropheryma whipplei).
        • Super rare causes of endocarditis with difficult to grow culture: Mycoplasma, Legionella, Bartonella, Brucella, HACEK organisms
        • TEE is positive in > 90% of cases of FUO from infective endocarditis.
      • Viral i.e. EBV
    • Malignancy: Most common are lymphoma and leukemia.
      • NH Lymphoma
      • Leukemia
      • RCC
      • HCC
      • Myelodysplastic syndromes
    • Systemic Rheumatic disease
      • Adult onset Still’s disease: young and middle age adults, daily fevers, arthritis, evanescent rash.
      • GCA: Older patients
      • Polyarteritis nodosa, Takayasu, GPA, cryoglobulinemia
    • Others
      • Drugs: Antibiotics, H1 & H2 blocking antihistamines, antiepileptic drugs, NSAIDS, hydralazine, antithyroid drugs, digoxin.
      • Factitious fever: Psych, predominantly affects F and healthcare professionals
      • Disordered heat homeostasis after a stroke or from hyperthyroidism
      • Dental abscess
      • Multiple concurrent infections
      • Alcoholic hepatitis
      • VTE/PE
      • Hematoma
      • Hereditary periodic fever syndromes
    • Unidentified: 19% of cases are unidentified.
  • Management/Diagnostic Principles
    • Get a detailed history, including fever pattern exposure history, sexual history, family history, medications.
    • Do not start empiric therapy unless pt is neutropenic or unstable, or you have a high-suspicions for GCA or culture negative endocarditis.

DLBCL

Epidemiology

  • Most common type of NH Lymphoma, representing 25% of cases
  • Median age: 64, 55% men. Also accounts for 25% of childhood NHL.
  • Caucasians at higher risk and esp patients of Swedish and Danish ancestry
  • Other risk factors: HIV, h/o radiation or chemotherapy

Pathophysiology

  • Heterogenous group of tumors that arise from mature B cells in (90% of cases, the other 10% from T cells)
  • Most common mutations found in DLBCL:
    • BCL6 gene mutation
    • BCL2 activation
    • MYC overexpression

Presentation

  • Nodal and extra-nodal manifestation at time of diagnosis. Most common extra-nodal manifestation is bonemarrow or GI tract.
  • Typically pts present with a mass, most commonly in the neck, abd, or mediastinum but it can manifest anywhere.
  • Painless LAD might be present in 2/3 of cases.
  • Less than 50% will have B-sx.
  • Can present with pancytopenia. Might see elevated LDH, uric acid, and calcium.

Diagnosis

  • Excision LN or tissue biopsy, excisional LN is preferred

Staging

  • Ann Arbor Criteria
  • AnnArbor.jpg
    • Stage I – disease in single lymph node or lymph node region.
    • Stage II – disease in two or more lymph node regions on same side of diaphragm. Note: Stage II contiguous means two or more lymph nodes in close proximity (side by side).
    • Stage III – disease in lymph node regions on both sides of the diaphragm are affected.
    • Stage IV – disease is wide spread, including multiple involvement at one or more extranodal (beyond the lymph node) sites, such as the bone marrow (which is involved commonly), liver, pleura (thin lining of the lungs).
    • Spleen is considered nodal

Management

    • 1st line is RCHOP (3 cycles) and local regional radiation, 6-8 cycles of R-CHOP is an acceptable alternative.
    • Emerging data, DA-EPOCH is better for younger patients < 60 yo and with certain phenotypes
    • Double Hit Lymphoma: Lymphoma resembling DLBCL but has MYC gene translocation AND rearrangement of BCL 2 or BCL 6. RCHOP still first line but overall prognosis is worse. DA-EPOCH-R might work better.

AST/ALT in thousands… Acute Hepatitis A! 3/12/2019

Thanks to Kevin and Brayden for presenting a 36yo F with no medical history presenting with acute abdominal pain, nausea, and anorexia. Her AST/ALTs were in the thousands and she was ultimately diagnosed with acute hepatitis A! Incidentally her HB Core Ab came back “borderline…”


AST ALT Elevation

  • If AST/ALTs are in the thousands, there are only a few entities that can cause this:
    • Ischemia (shock liver)
    • Toxins (Tylenol is most common), Amanita aka magic mushrooms, herbal supplements (we don’t know what they put in these!)
    • Acute viral hepatitis (HAV, HBV, HCV, HEV, HSV, CMV, VZV, parvovirus)
  • Less common:
    • Autoimmune hepatitis
    • Acute Budd Chiari
    • Reactivation HBV, HDV
    • HLH (we seem to see this a lot in this hospital for some reason?)
    • Malignant infiltration
    • HELLP
    • Wilsonian Crisis (severe hemolysis and impending acute liver failure in setting of Wilson’s)
  • For acute viral hepatitis, ALT is typically higher than AST.

Hepatitis A

Epidemiology

  • Global, 1.4 mil cases per year, can be sporadic or epidemic form
  • Fecal oral route, either person-to-person contact or ingestion of contaminated food or water.
  • Other risk factors: Sexual transmission (anal/oral sex), day care, consumption of raw or undercooked shellfish, veggies, or eating food prepared by an infected food handler.

Presentation

  • Incubation period: 15-50 days, average of 28 days.
  • Acute onset N/V, fever, anorexia, abd pain are typical.
  • Bilirubinuria, pale stools can also be seen within a few days.
  • Jaundice + pruritus. Jaundice peaks within 2 weeks.
  • Exam: Jaundice, hepatomegaly, RUQ pain.
  • Serum aminotransferases often > 1000 IU/dL, bili typically < 10, alk phos can be nrl to mildly elevated. ALT is commonly higher than AST.
  • Kids: Can be asymptomatic.

Diagnosis

  • Serum Anti-HAV IgM is diagnostic, detectable at time of symptom onset, remain detectable for 3-6 months after infection.
  • Anti-HAV IgG: remain detectable for decades, protective vs future infections. Detection of anti-HAV IgM and IgG reflects past infection or vaccination.

Management

  • Primarily supportive, but transfer to a transplant center might be indicated if pt goes into fulminant liver failure (severe acute liver injury with encephalopathy and impaired synthetic function i.e. INR >5 in patients without pre-existing liver disease)
  • Report to public health! Fax a confidential morbidity report over to Santa Clara County Department of Public Health

Vaccination

  • Single Antigen inactivated virus: 2 IM doses 6-18 months apart
  • Combo HAV and HBV inactivated virus vaccine: Adults only, 0, 1, 6 mo (3 doses total)

Prognosis

  • Generally pretty good, less than 1% go into fulminant hepatic failure.
  • Risk factors for severe complications: > 50, underlying liver dz
  • Other Complications
    • Relapsing hepatitis: Up to to 10% of pts experience a relapse of sx 6 months after the acute episode for ~ < 3 weeks. Multiple relapses can occur. These patients usually make a complete recovery
    • Autoimmune hepatitis: HAV can trigger development of autoimmune hepatitis.
    • Cholestatic hepatitis: Prolonged period of jaundice > 3 months, typically self-resolving

Hepatitis B serologies made ridiculously simple

Capture

Shingles and Complications 3/11/2019

Thanks Elan for presenting a case of a 91 year old F presenting with a progressively painful and erythematous rash, 2 weeks after she was treated with presumed Shingles by her PCP. It turned out that she had superimposed cellulitis over her healing Shingles lesions and possibly elements of post-herpetic neuralgia, requiring a Dilaudid PCA for pain control.

Lame joke of the day: Shingles + Cellulitis = Shinglelitis, get it?


Shingles

Epidemiology

  • Risk inc with age, esp for pts > 50, but it can develop at any age
  • Fortunately, most people will only have one outbreak in their life time, < 4% recurrence

Pathophysiology

  • Reactivation of the varicella zoster virus in sensory ganglia after a long latency period following primary infection from varicella (chicken pox). When the virus activates, the virus travels down the nerve fibers to the skin, hence a dermatomal distribution.
  • Weakening of the immune system is associated with outbreaks, i.e. AIDS, lymphoma, immune-suppressives.

Presentation

  • 2-3 days prior to rash: pt might develop a tingling sensation, hypersensitivity, or itching over a particular dermatome. Later on vesicles on an erythematous base develop. Painful and very sensitive.
  • Blisters form over 3-5 days, then dry and crust over the next 5 days
  • Blisters are CONTAGIOUS until the vesicles scab over.
    • Keep affected area dry and clean!
  • Expanding rash or blisters that persist for > 2 weeks indicate immune-compromised status

Complications

  • Most common is post-herpetic neuralgia
    • 10% of patients, inc with age
    • Pain can be very debilitating, some patients need to be admitted for pain control.
  • Zoster ophthalmicus
    • Involves the eye, seen in 10-25% of cases when shingles hit V1
    • Antiviral should be administered ASAP, preferably within 72 hours of onset of sx.
    • Valacyclovir is recommended, 7-day course, 1000mg PO TID
    • Alternative: Acyclovir 800mg PO 5 times daily x 7-10 days, Famciclovir 500mg PO TID.
    • If e/o keratitis or uveitis, topical steroids can be used.
    • Can lead to vision loss, especially with corneal scarring. Some patients would require corneal transplant.
    • Post-herpetic neuralgia occurs in 36.6% of pts over 60, and 47.5% over age 70.
  • Disseminated zoster
    • If > 3 contiguous dermatomes or 2 separated dermatomes are affected.
  • Bacterial infection of the skin:
    • Risks inc with scratching
    • Inc risk of scarring
  • Ramsey Hunt Syndrome:
    • Reactivation of VZV at the geniculate ganglion.
    • Triad of Ipsilateral facial paralysis, ear pain, vesicles on face/ear or IN THE EAR. Can lead to deafness, tinnitis or vertigo due to vestibulocochlear nerve involvement.
    • Mgx: Anti-viral within 72 hours, steroids. Hearing loss is likely permanent so treat ASAP.

Diagnosis

  • Primarily clinical
  • Swabbing ulcer/vesicular fluid for HSV PCR has high sensitivity, quick turn around time.

Management

  • Acute management
    • Anti-viral: Valacyclovir, famiciclovir, acyclovir. Start ASAP and preferably even before blisters occur. Effectiveness is greatest if antiviral is started within 72 hours of onset of symptoms (even before vesicles appear if clinical suspicion is high enough!)
    • IV antiviral recommended for disseminated disease
    • Options: Acyclovir (5 times a day dosing), Valacyclovir (TID dosing), famiciclovir (TID as well).
    • Help shorten duration and complications
    • Pain control:
      • Lidocaine, capsaicin, gabapentin, Lyrica.
      • Use opioids if and only if necessary.
      • Antidepressants i.e. Cymbalta and Effexor have variable benefits for post-herpetic neuralgia.
    • Keep area dry and clean, DO NOT SCRATCH.
  • Infection Control:
    • Localized herpes zoster: Standard precautions, contact
    • Disseminated: airborne + contact
    • Immunocompromised patient: airborne + contact regardless
  • Post-exposure:
    • Previously received 2 doses of varicella vaccine: Monitor for 8-21 days for sx
    • Previously only received 1 dose of varicella vaccine: Should get the 2nd dose ASAP (minimum of 4 weeks apart from 1st dose). Monitor for sx.
    • No prior vaccination: Potentially contagious from days 8-21 post exposure, should be removed from patient care duties. Post-exposure vaccination should be provided ASAP. If varicella vaccination is contraindicated (i.e. pregnant), varicella-zoster immune globulin is recommended.
  • Vaccination/Prevention
    • Vaccinate children
    • Vaccinate adults > 50 regardless of whether they have had chicken pox or shingles and regardless of whether they had the older vaccine
      • Older: Weakened live virus, Zostavax
      • Newer: Recombinant Herpes Zoster vaccine, Shingrix, 2 doses IM, 2-6 months apart, at least 2 months after the older vaccine. Contains inactivated parts of the virus, not a live vaccine.
        • Effectiveness: 97% effective in preventing shingles for pts > 50, vs Zostavax which is 50-64% effective.
        • Reduces post-herpetic neuralgia if you get it shingles

Cardiorenal Syndrome 3/5/2019

Thanks Elan for presenting a case of a 63yo M with HIV HFrEF (25%), EtOH cirrhosis (CP Class A, MELD 8), HTN, HLD, and ongoing alcohol use with dietary nonadherence presenting with shortness of breath and anasarca. His JVD was elevated on presentation, and CT PE/AP in the ED revealed dilated IVC and e/o pulmonary edema.

He underwent diuresis and initially improved, but 48 hours into his hospitalization, he developed oliguric AKI, hepatic encephalopathy, and relative hypotension.

Urine studies were consistent with activation of RAAS and ADH (kidneys seeing low perfusion, and echo was concerning for biventricular failure with EF < 20%. A trial of Lasix managed to produce a UOP of 800cc in 24 hours, so a decision was made to transfer pt to the Stepdown for dobutamine assisted diuresis for suspected Cardiorenal Syndrome. Pt ultimately diuresed 18L of fluid (his weight also went down 10+kg, that’s around 22lbs!) and his renal function quickly returned to baseline after aggressive diuresis.


Cardiorenal Syndrome

The diagnosis dilemma for this case was the etiology of pt’s AKI. He was exposed to contrast, hence 48 hours later contract-induced nephropathy can be expected. He also has liver cirrhosis with acute decompensation, hence hepatorenal syndrome (HRS) is something that we cannot miss. Given his poor cardiac function, cardiorenal syndrome (CRS) is also high on the differential!

Keep in mind that there are 5 types of Cardiorenal Syndrome:

  • Type 1: Acute heart failure -> AKI, decreased renal arterial flow due to acutely decompensated HF
  • Type 2: Chronic HF leading to chronic renal hypoperfusion leading to CKD
  • Type 3: AKI leading to adverse cardiac events
  • Type 4: CKD leading to adverse cardiac events
  • Type 5: Multifactorial, systemic insult leads to both cardiac and renal failure

Regardless, the general principle is to restore renal perfusion. Given his biventricular failure, volume status, and initial presentation, Cardiorenal is suspected as more likely, hence pt received inotropic support (improves forward flow) and diuresis (Get pt back on the right side of the Frank Starling curve, also improves forward flow). Overall management of CRS is not much different compared to acute decompensated heart failure.

There is some evidence that more aggressive diuresis is associated with better outcomes (ESCAPE trial).