https://wikem.org/w/api.php?action=feedcontributions&feedformat=atom&user=Mhankerson 2026-05-12T23:34:28Z User contributions MediaWiki 1.38.2 https://wikem.org/w/index.php?title=Hereditary_spherocytosis&diff=14778 2013-12-02T00:16:04Z

<p>Mhankerson: new article</p> <hr /> <div>==Introduction==<br /> *Hereditary Spherocytosis (HS) = hereditary hemolytic anemia due to defect in RBC cell membrane (mainly spectrin, ankyrin)<br /> **75% Autosomal Dominant, 25% Autosomal Recessive<br /> <br /> <br /> ==Pathophysiology==<br /> *Deficient/Nonfunctional RBC cell membrane proteins that connect the cell membrane skeleton to the lipid bilayer<br /> <br /> <br /> ==Clinical Presentation==<br /> *Classic triad: Anemia, Jaundice, Splenomegaly<br /> <br /> <br /> *Mild HS: <br /> **No anemia, normal retic count, little or no jaundice/splenomegaly<br /> **No RBC transfusions<br /> **Dx’d later in life<br /> *Moderate HS: <br /> **Anemic, elevated retic, elevated bili, maybe splenomegaly<br /> **May require RBC transfusions<br /> **Dx’d in infancy or early childhood<br /> *Severe HS: <br /> **Marked hemolysis, anemia, hyperbili, splenomegaly<br /> **Require regular RBC transfusions<br /> **Dx’d in infancy<br /> <br /> <br /> ==Work-Up==<br /> *Low Hb, elevated retic count, spherocytes on peripheral smear<br /> *Elevated MCHC (RBC membrane leaky causing RBC dehydration)<br /> *Osmotic fragility test, AGLT, EMA binding test, cryohemolysis<br /> **One study showed AGLT + EMA binding test identified all HS pts<br /> *Negative Coombs test<br /> <br /> <br /> ==Complications==<br /> *Cholelithiasis secondary to intravascular hemolysis causing development of bilirubin gallstones<br /> *Pseudohyperkalemia: K+ leaks out of RBCs after blood draw<br /> <br /> <br /> ==Treatment==<br /> *Folic acid<br /> *RBC transfusion<br /> *EPO<br /> *Splenectomy<br /> **As late as possible, preferably &gt;6 yo<br /> **Post-op need encapsulated bacteria prophy: Strep Pneumo, H Influenza, Neiserria Meningitidis<br /> **Possible higher risk of arterial/venous thrombosis in HS after splenectomy<br /> *Hematopoietic cell transplant (most agree risks outweigh benefits)<br /> <br /> <br /> ==See Also==<br /> *[[DIC]], [[TTP]], [[HUS]], [[Microangiopathic Hemolytic Anemia (MAHA)]]<br /> *[[HELLP]], [[HIT]], [[Paroxysmal Nocturnal Hemoglobinuria (PNH)]]<br /> <br /> <br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Microangiopathic_hemolytic_anemia&diff=14589 2013-11-29T23:08:13Z

<p>Mhankerson: </p> <hr /> <div>==Introduction==<br /> '''Microangiopathic hemolytic anemia (MAHA)''' = variety of conditions that result in damaged endothelium of small vessels causing platelet aggregation and fibrin deposition which leads to shearing forces within these small vessels causing an intravascular fragmentation hemolysis<br /> <br /> <br /> ==Diagnosis==<br /> *Clinical features + heme labs<br /> *May have bleeding and thrombosis<br /> <br /> <br /> ==DDx==<br /> *Most common causes: [[DIC]], [[TTP]], [[HUS]]<br /> *Other medical causes: [[malignant hypertension]], [[HELLP]], [[Antiphospholipid Syndrome (APS)]], [[scleroderma]], [[Paroxysmal Nocturnal Hemoglobinuria (PNH)]], malignancy, renal allograft rejection, vasculitides like [[polyarteritis nodosa]] and [[Wegener's granulomatosis]]<br /> *Drugs: chemotherapy; [[Plavix]] (clopidogrel) associated with [[TTP]]<br /> *Nonvascular causes: prosthetic valve (more common w/ mechanical, more common at aortic valve), [[LVAD]], [[TIPS]], coil embolization, patched AV shunt, [[AVM]]<br /> <br /> <br /> ==Work-Up==<br /> *Peripheral smear, hemoglobin, platelets, PT/INR, PTT, fibrinogen, FDPs, D-dimer, haptoglobin, LDH, bilirubin<br /> **Schistocytes (aka Helmet cells) secondary to fragmentation hemolysis classic finding on peripheral smear<br /> <br /> <br /> *All MAHAs = <br /> **Schistocytes<br /> **High: +/- LDH and bili<br /> **Low: Hgb, platelets, +/- haptoglobin<br /> <br /> <br /> *DIC = '''elevated''' PT/INR/PTT/FDPs/D-dimer, '''low''' fibrinogen<br /> <br /> *TTP/HUS = '''normal''' PT/INR/PTT/FDPs/D-dimer/fibrinogen<br /> <br /> <br /> ==See Also==<br /> *[[DIC]], [[TTP]], [[HUS]]<br /> *[[Malignant hypertension]], [[HELLP]], [[Antiphospholipid Syndrome (APS)]], [[Paroxysmal Nocturnal Hemoglobinuria (PNH)]]<br /> *[[HIT]]<br /> <br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Antiphospholipid_syndrome&diff=14588 2013-11-29T23:06:51Z

<p>Mhankerson: </p> <hr /> <div>==Introduction==<br /> *APS definition (need 1 from each category): <br /> **Presence of at least 1 of the following: DVT, arterial thrombosis, or pregnancy morbidity (eg fetal loss, preterm)<br /> **Presence of at least 1 of the following antiphospholipid antibodies (aPL): lupus anticoagulant (LA), anticardiolipin (aCL), β2-glycoprotein-1 (β2-GP-1)<br /> <br /> <br /> *APS can occur as a primary condition or in setting of underlying disease (eg SLE)<br /> <br /> <br /> ==Pathophysiology==<br /> *Currently accepted theory: Susceptible pts (eg SLE) develop aPL after infection. After development of aPL, “second hit” stress required to develop full-blown APS. aPL affects coagulation by interacting with protein C, annexin V, platelets, proteases, tissue factor, and impairing finbrinolysis<br /> **“Second hit” stressors: smoking, prolonged immobilization, pregnancy, exogenous estrogen, malignancy, nephrotic syndrome, HTN, hyperlipidemia<br /> <br /> <br /> ==Diagnosis==<br /> *Presence of DVT, arterial thrombus, or pregnancy morbidity (eg fetal loss, preterm)<br /> *Presence of aPL<br /> <br /> <br /> ==Clinical Manifestations==<br /> *Thrombocytopenia, increased PT/INR and aPTT<br /> *[[Microangiopathic Hemolytic Anemia (MAHA)]]<br /> *DVT/PE<br /> *Fetal loss<br /> *Heart valve disease<br /> *aPL-nephropathy<br /> *Stroke/TIA, other neuro sx<br /> *Livedo reticularis<br /> <br /> <br /> ==Complications==<br /> *Catastrophic APS: widespread thrombotic disease w/ multiorgan failure precipitated by some stress (eg infection)<br /> <br /> <br /> ==APS Treatment==<br /> *Anticoagulation (unfractionated heparin, LMWH, or warfarin)<br /> **No benefit in treatment or prophy using ASA or plavix<br /> **Add hydroxychloroquine if pt has SLE<br /> **Warfarin contraindicated in pregnancy!<br /> <br /> <br /> *IVIG, plasmapharesis, and steroids have not been proven to be of benefit in APS<br /> <br /> <br /> ==Catastrophic APS Treatment==<br /> *Treat stress that preceipitated catastrophic APS (eg infection), anticoagulation, high dose steroids<br /> **If evidence of microangiopathy (thrombocytopenia, MAHA), add IVIG and plasma exchange to above regimen<br /> <br /> <br /> ==See Also==<br /> *[[DIC]], [[TTP]], [[HUS]], [[Microangiopathic Hemolytic Anemia (MAHA)]]<br /> *[[HELLP]], [[Paroxysmal Nocturnal Hemoglobinuria (PNH)]], [[HIT]]<br /> <br /> [[Category:Heme/Onc]] [[Category:Rheum]]</div>

Mhankerson https://wikem.org/w/index.php?title=Paroxysmal_nocturnal_hemoglobinuria&diff=14587 2013-11-29T23:06:06Z

<p>Mhankerson: new article</p> <hr /> <div>==Introduction==<br /> PNH = Intravascular hemolysis caused by increased sensitivity of RBCs to hemolytic action of complement<br /> <br /> <br /> ==Pathophysiology==<br /> *Abnormal PIG-A gene &gt; defect in GPI-linked anchor &gt; partial/complete absence of GPI-linked proteins (mainly CD55 and CD59) &gt; increased sensitivity of RBCs to hemolytic action of complement<br /> <br /> <br /> *Hemolysis precipitated by stresses that activate complement (eg infection)<br /> **Nocturnal hemolysis attributed to intestinal absorption of lipopolysaccharide (strong activator of complement) at night<br /> <br /> <br /> ==Diagnosis==<br /> *Anemia<br /> *Negative Coombs test<br /> *Hemoglobinuria<br /> *Elevated LDH<br /> *Decreased haptoglobin<br /> *Positive sucrose lysis test or Ham test (both test sensitivity of RBCs to lysis by complement)<br /> *Other clues: granulocytopenia/thrombocytopenia, venous thrombosis, aplastic anemia, MDS, dysphagia or abdominal pain<br /> <br /> <br /> ==Clinical Manifestations==<br /> *Intravascular hemolysis<br /> *Renal failure (both from intravascular hemolysis causing AKI and chronic hemolysis causing iron deposition in kidneys)<br /> *DVT, thrombosis of hepatic/intraabdominal/cerebral veins, arterial thrombosis<br /> *Bone marrow failure leading to aplastic anemia<br /> *Myelodysplastic (MDS) or myeloproliferative disorders<br /> *Acute leukemia<br /> *Esophageal spasm<br /> *Crampy abdominal pain<br /> *Impotence/ED<br /> <br /> <br /> ==Treatment==<br /> *Eculizumab (C5 antibody): stops hemolysis in PNH<br /> *Iron/folate supplements<br /> *RBC transfusion PRN<br /> *Prednisone may decrease RBC destruction<br /> *For severe hematopoietic dysfunction w/ marked cytopenias: hematopoietic cell transplant or immunosuppression (cyclosporine or antithymocyte globulin)<br /> *Anticoagulation for thrombosis<br /> <br /> <br /> ==See Also==<br /> *[[DIC]], [[TTP]], [[HUS]], [[Microangiopathic Hemolytic Anemia (MAHA)]]<br /> *[[HELLP]], [[HIT]], [[Hereditary Sperocytosis (HS)]]<br /> <br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Antiphospholipid_syndrome&diff=14586 2013-11-29T22:04:23Z

<p>Mhankerson: edit</p> <hr /> <div>==Introduction==<br /> *APS definition (need 1 from each category): <br /> **Presence of at least 1 of the following: DVT, arterial thrombosis, or pregnancy morbidity (eg fetal loss, preterm)<br /> **Presence of at least 1 of the following antiphospholipid antibodies (aPL): lupus anticoagulant (LA), anticardiolipin (aCL), β2-glycoprotein-1 (β2-GP-1)<br /> <br /> <br /> *APS can occur as a primary condition or in setting of underlying disease (eg SLE)<br /> <br /> <br /> ==Pathophysiology==<br /> *Currently accepted theory: Susceptible pts (eg SLE) develop aPL after infection. After development of aPL, “second hit” stress required to develop full-blown APS. aPL affects coagulation by interacting with protein C, annexin V, platelets, proteases, tissue factor, and impairing finbrinolysis<br /> **“Second hit” stressors: smoking, prolonged immobilization, pregnancy, exogenous estrogen, malignancy, nephrotic syndrome, HTN, hyperlipidemia<br /> <br /> <br /> ==Diagnosis==<br /> *Presence of DVT, arterial thrombus, or pregnancy morbidity (eg fetal loss, preterm)<br /> *Presence of aPL<br /> <br /> <br /> ==Clinical Manifestations==<br /> *Thrombocytopenia, increased PT/INR and aPTT<br /> *[[Microangiopathic Hemolytic Anemia (MAHA)]]<br /> *DVT/PE<br /> *Fetal loss<br /> *Heart valve disease<br /> *aPL-nephropathy<br /> *Stroke/TIA, other neuro sx<br /> *Livedo reticularis<br /> <br /> <br /> ==Complications==<br /> *Catastrophic APS: widespread thrombotic disease w/ multiorgan failure precipitated by some stress (eg infection)<br /> <br /> <br /> ==APS Treatment==<br /> *Anticoagulation (unfractionated heparin, LMWH, or warfarin)<br /> **No benefit in treatment or prophy using ASA or plavix<br /> **Add hydroxychloroquine if pt has SLE<br /> **Warfarin contraindicated in pregnancy!<br /> <br /> <br /> *IVIG, plasmapharesis, and steroids have not been proven to be of benefit in APS<br /> <br /> <br /> ==Catastrophic APS Treatment==<br /> *Treat stress that preceipitated catastrophic APS (eg infection), anticoagulation, high dose steroids<br /> **If evidence of microangiopathy (thrombocytopenia, MAHA), add IVIG and plasma exchange to above regimen<br /> <br /> <br /> ==See Also==<br /> *[[DIC]], [[TTP]], [[HUS]], [[Microangiopathic Hemolytic Anemia (MAHA)]]<br /> *[[HELLP]], [[PNH]], [[HIT]]<br /> <br /> [[Category:Heme/Onc]] [[Category:Rheum]]</div>

Mhankerson https://wikem.org/w/index.php?title=Microangiopathic_hemolytic_anemia&diff=14585 2013-11-29T22:03:36Z

<p>Mhankerson: edit</p> <hr /> <div>==Introduction==<br /> '''Microangiopathic hemolytic anemia (MAHA)''' = variety of conditions that result in damaged endothelium of small vessels causing platelet aggregation and fibrin deposition which leads to shearing forces within these small vessels causing an intravascular fragmentation hemolysis<br /> <br /> <br /> ==Diagnosis==<br /> *Clinical features + heme labs<br /> *May have bleeding and thrombosis<br /> <br /> <br /> ==DDx==<br /> *Most common causes: [[DIC]], [[TTP]], [[HUS]]<br /> *Other medical causes: [[malignant hypertension]], [[HELLP]], [[Antiphospholipid Syndrome (APS)]], [[scleroderma]], [[PNH]], malignancy, renal allograft rejection, vasculitides like [[polyarteritis nodosa]] and [[Wegener's granulomatosis]]<br /> *Drugs: chemotherapy; [[Plavix]] (clopidogrel) associated with [[TTP]]<br /> *Nonvascular causes: prosthetic valve (more common w/ mechanical, more common at aortic valve), [[LVAD]], [[TIPS]], coil embolization, patched AV shunt, [[AVM]]<br /> <br /> <br /> ==Work-Up==<br /> *Peripheral smear, hemoglobin, platelets, PT/INR, PTT, fibrinogen, FDPs, D-dimer, haptoglobin, LDH, bilirubin<br /> **Schistocytes (aka Helmet cells) secondary to fragmentation hemolysis classic finding on peripheral smear<br /> <br /> <br /> *All MAHAs = <br /> **Schistocytes<br /> **High: +/- LDH and bili<br /> **Low: Hgb, platelets, +/- haptoglobin<br /> <br /> <br /> *DIC = '''elevated''' PT/INR/PTT/FDPs/D-dimer, '''low''' fibrinogen<br /> <br /> *TTP/HUS = '''normal''' PT/INR/PTT/FDPs/D-dimer/fibrinogen<br /> <br /> <br /> ==See Also==<br /> *[[DIC]], [[TTP]], [[HUS]]<br /> *[[Malignant hypertension]], [[HELLP]], [[Antiphospholipid Syndrome (APS)]], [[PNH]]<br /> *[[HIT]]<br /> <br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Thrombotic_thrombocytopenic_purpura&diff=14584 2013-11-29T22:02:16Z

<p>Mhankerson: </p> <hr /> <div>==Background==<br /> *Pathophysiology<br /> **Insufficient ADAMTS-13 activity allows vWF multimers to accumulate in microcirculation<br /> ***Leads to platelet aggregation/thrombocytopenia and hemolysis of RBCs<br /> *Similar to but different from [[HUS]] (which is more common in peds)<br /> *[[Microangiopathic Hemolytic Anemia (MAHA)]] + low plts is TTP until proven otherwise<br /> *Can occur as a result of [[Plavix]] (clopidogrel) use (usually within first 2 wk of starting)<br /> <br /> ===Risk Factors===<br /> *Congenitally deficient ADAMTS-13 activity and:<br /> #Pregnancy<br /> #Infection<br /> #Inflammation<br /> #Medication use (quinolones, ticlopidine, clopidogrel)<br /> <br /> ==Clinical Features==<br /> *Pentad<br /> #[[Microangiopathic Hemolytic Anemia (MAHA)]]<br /> #Thrombocytopenia<br /> #Fever<br /> #Renal pathology<br /> #CNS abnormalities (seizure, AMS, CVA, coma)<br /> <br /> *TTP pentad mnemonic = FAT RN<br /> **Fever, Anemia, Thrombocytopenia, Renal, Neuro sx<br /> <br /> ==DDX==<br /> *Other MAHAs (eg, [[HUS]], [[DIC]], [[malignant hypertension]])<br /> *[[ITP]]<br /> *[[Sepsis]]<br /> *[[SLE]]<br /> *[[HELLP]] syndrome<br /> **Difficult to distinguish<br /> **Anemia, plt count, and LDH tend to be more severe in TTP; LFTs more severe in HELLP<br /> <br /> == Work-Up ==<br /> <br /> *CBC with peripheral smear (anemia, '''schistocytes''', thrombocytopenia)<br /> *LDH (elevated)<br /> *Haptoglobin (decreased)<br /> *Reticulocyte count (appropriate)<br /> *UA (hemoglobinuria) <br /> *Creatinine (possibly elevated)<br /> *LFTs (increased bilirubin) <br /> *PT/PTT/INR (normal; differentiates from [[DIC]]) <br /> *Urine pregnancy (significant association between pregnancy and TTP)<br /> <br /> == Treatment ==<br /> <br /> *Plasma exchange (plasmapheresis) <br /> **Replaces defective or insufficient ADAMTS-13 and clears vWF multimers <br /> *Transfusion <br /> **Indicated if plasma exchange cannot be performed immediately <br /> **FFP <br /> **Platelet (only for life-threatening bleeding or intracranial hemorrhage) <br /> ***Platelet infusion may lead to acutely worsened thrombosis, renal failure, and death<br /> *Splenectomy - 2nd line therapy<br /> <br /> ==Disposition==<br /> *Admit for plasma exchange<br /> <br /> ==See Also==<br /> *[[Microangiopathic Hemolytic Anemia (MAHA)]], [[HUS]], [[DIC]]<br /> *[[HELLP]], [[SLE]], [[Antiphospholipid Syndrome (APS)]]<br /> *[[ITP]]<br /> <br /> ==Source ==<br /> *Tintinalli<br /> *Harwood Nuss<br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Thrombotic_thrombocytopenic_purpura&diff=14583 2013-11-29T21:59:51Z

<p>Mhankerson: edit</p> <hr /> <div>==Background==<br /> *Pathophysiology<br /> **Insufficient ADAMTS-13 activity allows vWF multimers to accumulate in microcirculation<br /> ***Leads to platelet aggregation/thrombocytopenia and hemolysis of RBCs<br /> *Similar to but different from [[HUS]] (which is more common in peds)<br /> *[[Microangiopathic Hemolytic Anemia (MAHA)]] + low plts is TTP until proven otherwise<br /> *Can occur as a result of [[Plavix]] (clopidogrel) use (usually within first 2 wk of starting)<br /> <br /> ===Risk Factors===<br /> *Congenitally deficient ADAMTS-13 activity and:<br /> #Pregnancy<br /> #Infection<br /> #Inflammation<br /> #Medication use (quinolones, ticlopidine, clopidogrel)<br /> <br /> ==Clinical Features==<br /> *Pentad<br /> #[[Microangiopathic Hemolytic Anemia (MAHA)]]<br /> #Thrombocytopenia<br /> #Fever<br /> #Renal pathology<br /> #CNS abnormalities (seizure, AMS, CVA, coma)<br /> <br /> *TTP pentad mnemonic = FAT RN<br /> **Fever, Anemia, Thrombocytopenia, Renal, Neuro sx<br /> <br /> ==DDX==<br /> *Other MAHAs (eg, [[HUS]], [[DIC]], [[malignant hypertension]])<br /> *[[ITP]]<br /> *[[Sepsis]]<br /> *[[SLE]]<br /> *[[HELLP]] syndrome<br /> **Difficult to distinguish<br /> **Anemia, plt count, and LDH tend to be more severe in TTP; LFTs more severe in HELLP<br /> <br /> == Work-Up ==<br /> <br /> *CBC with peripheral smear (anemia, '''schistocytes''', thrombocytopenia)<br /> *LDH (elevated)<br /> *Haptoglobin (decreased)<br /> *Reticulocyte count (appropriate)<br /> *UA (hemoglobinuria) <br /> *Creatinine (possibly elevated)<br /> *LFTs (increased bilirubin) <br /> *PT/PTT/INR (normal; differentiates from [[DIC]]) <br /> *Urine pregnancy (significant association between pregnancy and TTP)<br /> <br /> == Treatment ==<br /> <br /> *Plasma exchange (plasmapheresis) <br /> **Replaces defective or insufficient ADAMTS-13 and clears vWF multimers <br /> *Transfusion <br /> **Indicated if plasma exchange cannot be performed immediately <br /> **FFP <br /> **Platelet (only for life-threatening bleeding or intracranial hemorrhage) <br /> ***Platelet infusion may lead to acutely worsened thrombosis, renal failure, and death<br /> *Splenectomy - 2nd line therapy<br /> <br /> ==Disposition==<br /> *Admit for plasma exchange<br /> <br /> ==See Also==<br /> *[[Microangiopathic Hemolytic Anemia (MAHA)]], [[HUS]], [[DIC]]<br /> *[[HELLP]], [[SLE]], [[antiphospholipid syndrome]]<br /> *[[ITP]]<br /> <br /> ==Source ==<br /> *Tintinalli<br /> *Harwood Nuss<br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Antiphospholipid_syndrome&diff=14582 2013-11-29T21:56:52Z

<p>Mhankerson: new article</p> <hr /> <div>==Introduction==<br /> *APS definition (need 1 from each category): <br /> **Presence of at least 1 of the following: DVT, arterial thrombosis, or pregnancy morbidity (eg fetal loss, preterm)<br /> **Presence of at least 1 of the following antiphospholipid antibodies (aPL): lupus anticoagulant (LA), anticardiolipin (aCL), β2-glycoprotein-1 (β2-GP-1)<br /> <br /> <br /> *APS can occur as a primary condition or in setting of underlying disease (eg SLE)<br /> <br /> <br /> ==Pathophysiology==<br /> *Currently accepted theory: Susceptible pts (eg SLE) develop aPL after infection. After development of aPL, “second hit” stress required to develop full-blown APS. aPL affects coagulation by interacting with protein C, annexin V, platelets, proteases, tissue factor, and impairing finbrinolysis<br /> **“Second hit” stressors: smoking, prolonged immobilization, pregnancy, exogenous estrogen, malignancy, nephrotic syndrome, HTN, hyperlipidemia<br /> <br /> <br /> ==Diagnosis==<br /> *Presence of DVT, arterial thrombus, or pregnancy morbidity (eg fetal loss, preterm)<br /> *Presence of aPL<br /> <br /> <br /> ==Clinical Manifestations==<br /> *Thrombocytopenia, increased PT/INR and aPTT<br /> *[[Microangiopathic hemolytic anemia (MAHA)]]<br /> *DVT/PE<br /> *Fetal loss<br /> *Heart valve disease<br /> *aPL-nephropathy<br /> *Stroke/TIA, other neuro sx<br /> *Livedo reticularis<br /> <br /> <br /> ==Complications==<br /> *Catastrophic APS: widespread thrombotic disease w/ multiorgan failure precipitated by some stress (eg infection)<br /> <br /> <br /> ==APS Treatment==<br /> *Anticoagulation (unfractionated heparin, LMWH, or warfarin)<br /> **No benefit in treatment or prophy using ASA or plavix<br /> **Add hydroxychloroquine if pt has SLE<br /> **Warfarin contraindicated in pregnancy!<br /> <br /> <br /> *IVIG, plasmapharesis, and steroids have not been proven to be of benefit in APS<br /> <br /> <br /> ==Catastrophic APS Treatment==<br /> *Treat stress that preceipitated catastrophic APS (eg infection), anticoagulation, high dose steroids<br /> **If evidence of microangiopathy (thrombocytopenia, MAHA), add IVIG and plasma exchange to above regimen<br /> <br /> <br /> ==See Also==<br /> *[[DIC]], [[TTP]], [[HUS]], [[microangiopathic hemolytic anemia (MAHA)]]<br /> *[[HELLP]], [[PNH]], [[HIT]]<br /> <br /> [[Category:Heme/Onc]] [[Category:Rheum]]</div>

Mhankerson https://wikem.org/w/index.php?title=Microangiopathic_hemolytic_anemia&diff=14581 2013-11-29T21:47:13Z

<p>Mhankerson: </p> <hr /> <div>==Introduction==<br /> '''Microangiopathic hemolytic anemia (MAHA)''' = variety of conditions that result in damaged endothelium of small vessels causing platelet aggregation and fibrin deposition which leads to shearing forces within these small vessels causing an intravascular fragmentation hemolysis<br /> <br /> <br /> ==Diagnosis==<br /> *Clinical features + heme labs<br /> *May have bleeding and thrombosis<br /> <br /> <br /> ==DDx==<br /> *Most common causes: [[DIC]], [[TTP]], [[HUS]]<br /> *Other medical causes: [[malignant hypertension]], [[HELLP]], [[antiphospholipid syndrome]], [[scleroderma]], [[PNH]], malignancy, renal allograft rejection, vasculitides like [[polyarteritis nodosa]] and [[Wegener's granulomatosis]]<br /> *Drugs: chemotherapy; [[Plavix]] (clopidogrel) associated with [[TTP]]<br /> *Nonvascular causes: prosthetic valve (more common w/ mechanical, more common at aortic valve), [[LVAD]], [[TIPS]], coil embolization, patched AV shunt, [[AVM]]<br /> <br /> <br /> ==Work-Up==<br /> *Peripheral smear, hemoglobin, platelets, PT/INR, PTT, fibrinogen, FDPs, D-dimer, haptoglobin, LDH, bilirubin<br /> **Schistocytes (aka Helmet cells) secondary to fragmentation hemolysis classic finding on peripheral smear<br /> <br /> <br /> *All MAHAs = <br /> **Schistocytes<br /> **High: +/- LDH and bili<br /> **Low: Hgb, platelets, +/- haptoglobin<br /> <br /> <br /> *DIC = '''elevated''' PT/INR/PTT/FDPs/D-dimer, '''low''' fibrinogen<br /> <br /> *TTP/HUS = '''normal''' PT/INR/PTT/FDPs/D-dimer/fibrinogen<br /> <br /> <br /> ==See Also==<br /> *[[DIC]], [[TTP]], [[HUS]]<br /> *[[Malignant hypertension]], [[HELLP]], [[antiphospholipid syndrome]], [[PNH]]<br /> *[[HIT]]<br /> <br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Blood_products&diff=14063 2013-11-09T20:03:12Z

<p>Mhankerson: edit</p> <hr /> <div>==Packed Red Blood Cells==<br /> ===Features===<br /> #Can give type O Rh-positive pRBCs to a man or woman no longer of child-bearing age<br /> #Options:<br /> ###Leukocyte reduced<br /> ####Eliminates 70-85% of leukocytes<br /> ####Reduces nonhemolytic febrile reactions<br /> ####Prevents sensitization in pts who may require bone marrow transplant<br /> ####Minimizes risk of HIV and CMV infection<br /> ###Irradiated<br /> ####Eliminates capacity of T-cells to proliferate (prevents graft-versus-host disease)<br /> ####Consider in transplant pts, neonates and immunocompromised pts<br /> ###Washed<br /> ####Indicated for pts w/ hypersensitivity to plasma (such as IgA deficiency)<br /> <br /> ===Indications===<br /> #Acute hemorrhage or chronic anemia with Hb &lt;6<br /> #Symptomatic anemia or cardiopulmonary disease AND Hb &lt;10<br /> <br /> ===Dose===<br /> #One unit (250mL) raises hemoglobin by 1 g/dl<br /> ##Usually transfuse at least 2 units at a time (15mL/kg in peds)<br /> #Must transfuse no slower than 1 unit/4hr<br /> ##If require slower transfusion (e.g. risk for volume overload) the pRBC can be split<br /> <br /> ==Platelets==<br /> ===Features===<br /> #Transfusion should be type specific b/c platelets are bathed in plasma<br /> ##Non-type specific plts can be used but results in higher rate of complications<br /> #Like pRBCs, plts can be leukocyte reduced or washed<br /> <br /> ===Indications===<br /> #Plt count &lt;10K in asymptomatic patients (unless due to ITP, TTP, or HIT)<br /> #Plt count &lt;15K with a coagulation disorder or minor bleeding<br /> #Plt count &lt;20K with major bleeding<br /> #Plt count &lt;50K with need for invasive procedure or surgery<br /> #Plt count &lt;100K with need for neurologic or cardiac surgery<br /> <br /> ===Dose===<br /> #1 unit raises count by 50K<br /> <br /> ==Fresh Frozen Plasma==<br /> ===Features===<br /> #Contains all coagulation factors and fibrinogen<br /> ##40 mL/kg raises any factor by 100% (each unit is ~200mL)<br /> #May cause fluid overload<br /> #ABO compatibilty a must but crossmatch before transfusing not<br /> #INR of FFP is ~1.2<br /> <br /> ===Indications===<br /> #Rapid reversal of warfarin over-anticoagulation<br /> #Bleeding and multiple coagulation defects<br /> #Correction of coagulation defects for which no specific factor is available<br /> #Transfusion of more than one blood volume w/ evidence of active bleeding + coagulopathy<br /> <br /> ===Dose===<br /> #Transfuse at least 15 mL/kg at a time (4 units in 70-kg adult)<br /> <br /> ==Cryoprecipitate==<br /> ===Features===<br /> #Cold insoluble protein fraction of FFP<br /> #Contains: fibrinogen, vWF, and factor VIII<br /> #1 bag (10ml) has 50-500 units of factor 8 activity<br /> <br /> ===Indications===<br /> #Bleeding with fibrinogen level of &lt;100 milligrams/dL<br /> #Dysfibrinogenemia<br /> #Bleeding in vWD that is unresponsive to DDAVP and Factor VIII is unavailable (can also use Humate-P, FFP doesn't work well)<br /> <br /> ===Dose===<br /> #1 unit/5kg (usually 10 units are given at a time)<br /> ##Will raise fibrinogen level by 75<br /> <br /> ==Humate-P==<br /> ===Features===<br /> #Contains: vWF and factor VIII<br /> <br /> ===Indications===<br /> #Hemophilia A (can also use factor VIII, FFP doesn't work well)<br /> #vWD that is unresponsive to DDAVP (can also use cryo, FFP doesn't work well)<br /> <br /> ===Dose===<br /> Depends on condition and severity of bleeding<br /> <br /> ==See Also==<br /> *[[Transfusion Reactions]]<br /> *[[TXA]]<br /> <br /> ==Source==<br /> Tintinalli<br /> <br /> [[Category:Drugs]]<br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Malignant_Hypertension&diff=14062 2013-11-09T17:59:42Z

<p>Mhankerson: new article</p> <hr /> <div>==Pathophysiology==<br /> *Rapid increase in BP leading to severe HTN causing disruption of vascular endothelium which narrows/obliterates vascular lumen<br /> *RAAS activation<br /> *Autoregulation of BP lost<br /> <br /> ==Clinical Features==<br /> *Retinal hemorrhage and exudates, papilledema<br /> *Malignant nephrosclerosis causes AKI, proteinuria, hematuria<br /> *Neurologic sx due to [[hypertensive encephalopathy]], [[SAH]], lacunar infarcts<br /> **[[Hypertensive encephalopathy]] = cerebral edema secondary to breakthrough hyperperfusion from severe/sudden rise in BP (CPP autoregulation lost)<br /> *Can cause [[microangiopathic hemolytic anemia (MAHA)]]<br /> <br /> ==Diagnosis==<br /> *BP, physical exam, Cr, UA, +/- CT Head or MRI Brain<br /> <br /> ==Treatment==<br /> *IV BP meds: nitroprusside, nicardipine, labetalol, fenoldopam<br /> *If no IV meds: sublingual nifedipine or sublingual captopril; these can rapidly decrease BP in 10-30 min, beware of MI/stroke<br /> *Goal: Lower BP by 25% over 2-6hr, goal DBP 100-105<br /> <br /> ==See Also==<br /> *[[Hypertensive emergency]], [[Hypertensive encephalopathy]]<br /> *[[Microangiopathic hemolytic anemia (MAHA)]]<br /> <br /> [[Category:Cards]] [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Heparin-induced_thrombocytopenia&diff=14061 2013-11-09T17:16:44Z

<p>Mhankerson: edit</p> <hr /> <div>==Background==<br /> *Despite low plt count pt is actually hypercoagulable; bleeding is unusual <br /> *Pathophysiology<br /> **Pathologic activation / consumption of platelets due to Ab against heparin-plt complex<br /> **Activated platelets then cause blood clot formation<br /> ***Platelet count falls b/c plts are bound in clots<br /> **Can be caused by unfrationated or LMWH (10x common in the former)<br /> ***Occurs in 0.5-5% of pts tx'd w/ heparin<br /> *Thrombosis occurs in 35-75% of pts; 20-30% die w/in 1 month<br /> <br /> ==Clinical Features==<br /> *Typical<br /> **Symptoms begin 5-10d after initiation of heparin<br /> ***&gt;50% decrease in plt count (median nadir is ~60K; rarely &lt;20K)<br /> ***DVT or PE<br /> ***Cerebral vein or adrenal vein thrombosis<br /> ***Limb arterial occlusion<br /> ***CVA<br /> ***MI<br /> ***Skin necrosis<br /> *Rapid onset<br /> **Symptoms begin within hours of initiation of heparin<br /> ***Due to preexisting circulating antibody from sensitization several weeks earlier<br /> ***Sudden drop in plt count<br /> ***Thrombosis<br /> ***Flushing<br /> ***Tachycardia<br /> ***Hypotension<br /> ***Dyspnea<br /> *Delayed onset<br /> **Symptoms begin several days after heparin stopped<br /> **Severe thromboses<br /> <br /> ==Diagnosis==<br /> *Serotonin release assay (SRA) = gold standard<br /> **Positivity determined by optical density (OD) reported w/ assay (same concept as a titer)<br /> ***OD &lt;1 = &lt;5% chance of HIT<br /> ***OD 1.4 = 50% chance of HIT<br /> ***OD &gt;2 = 90% chance of HIT<br /> <br /> ==Treatment==<br /> #Discontinue all heparin products <br /> #Do not give platelts (may precipitate thrombosis)<br /> #Start anticoagulation<br /> ##Consider direct thrombin inhibitor [lepirudin (unless renal failure), argatroban (unless hepatobiliary disease), bivalirudin] or direct Xa inhibitor (fondaparinux, danaparoid)<br /> ##Avoid warfarin until platelets &gt;100K-150K<br /> <br /> ==See Also==<br /> *[[Heparin (Unfractionated)]]<br /> *[[Low Molecular Weight Heparin]]<br /> <br /> ==Dispostion==<br /> *Admit<br /> <br /> ==Source==<br /> Tintinalli<br /> <br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Thrombotic_thrombocytopenic_purpura&diff=14060 2013-11-09T16:51:01Z

<p>Mhankerson: edit</p> <hr /> <div>==Background==<br /> *Pathophysiology<br /> **Insufficient ADAMTS-13 activity allows vWF multimers to accumulate in microcirculation<br /> ***Leads to platelet aggregation/thrombocytopenia and hemolysis of RBCs<br /> *Similar to but different from [[HUS]] (which is more common in peds)<br /> *[[Microangiopathic hemolytic anemia]] + low plts is TTP until proven otherwise<br /> *Can occur as a result of [[Plavix]] (clopidogrel) use (usually within first 2 wk of starting)<br /> <br /> ===Risk Factors===<br /> *Congenitally deficient ADAMTS-13 activity and:<br /> #Pregnancy<br /> #Infection<br /> #Inflammation<br /> #Medication use (quinolones, ticlopidine, clopidogrel)<br /> <br /> ==Clinical Features==<br /> *Pentad<br /> #[[Microangiopathic hemolytic anemia (MAHA)]]<br /> #Thrombocytopenia<br /> #Fever<br /> #Renal pathology<br /> #CNS abnormalities (seizure, AMS, CVA, coma)<br /> <br /> *TTP pentad mnemonic = FAT RN<br /> **Fever, Anemia, Thrombocytopenia, Renal, Neuro sx<br /> <br /> ==DDX==<br /> *Other microangiopathic hemolytic anemias (eg, [[HUS]], [[DIC]], [[malignant hypertension]])<br /> *[[ITP]]<br /> *[[Sepsis]]<br /> *[[SLE]]<br /> *[[HELLP]] syndrome<br /> **Difficult to distinguish<br /> **Anemia, plt count, and LDH tend to be more severe in TTP; LFTs more severe in HELLP<br /> <br /> == Work-Up ==<br /> <br /> *CBC with peripheral smear (anemia, '''schistocytes''', thrombocytopenia)<br /> *LDH (elevated)<br /> *Haptoglobin (decreased)<br /> *Reticulocyte count (appropriate)<br /> *UA (hemoglobinuria) <br /> *Creatinine (possibly elevated)<br /> *LFTs (increased bilirubin) <br /> *PT/PTT/INR (normal; differentiates from [[DIC]]) <br /> *Urine pregnancy (significant association between pregnancy and TTP)<br /> <br /> == Treatment ==<br /> <br /> *Plasma exchange (plasmapheresis) <br /> **Replaces defective or insufficient ADAMTS-13 and clears vWF multimers <br /> *Transfusion <br /> **Indicated if plasma exchange cannot be performed immediately <br /> **FFP <br /> **Platelet (only for life-threatening bleeding or intracranial hemorrhage) <br /> ***Platelet infusion may lead to acutely worsened thrombosis, renal failure, and death<br /> *Splenectomy - 2nd line therapy<br /> <br /> ==Disposition==<br /> *Admit for plasma exchange<br /> <br /> ==See Also==<br /> *[[Microangiopathic hemolytic anemia]], [[HUS]], [[DIC]]<br /> *[[HELLP]], [[SLE]], [[antiphospholipid syndrome]]<br /> *[[ITP]]<br /> <br /> ==Source ==<br /> *Tintinalli<br /> *Harwood Nuss<br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Thrombotic_thrombocytopenic_purpura&diff=14059 2013-11-09T16:42:41Z

<p>Mhankerson: edit</p> <hr /> <div>==Background==<br /> *Pathophysiology<br /> **Insufficient ADAMTS-13 activity allows vWF multimers to accumulate in microcirculation<br /> ***Leads to platelet aggregation/thrombocytopenia and hemolysis of RBCs<br /> *Similar to but different from [[HUS]] (which is more common in peds)<br /> *[[Microangiopathic hemolytic anemia]] + low plts is TTP until proven otherwise<br /> *Can occur as a result of [[Plavix]] (clopidogrel) use (usually within first 2 wk of starting)<br /> <br /> ===Risk Factors===<br /> *Congenitally deficient ADAMTS-13 activity and:<br /> #Pregnancy<br /> #Infection<br /> #Inflammation<br /> #Medication use (quinolones, ticlopidine, clopidogrel)<br /> <br /> ==Clinical Features==<br /> *Pentad<br /> #[[Microangiopathic hemolytic anemia]]<br /> #Thrombocytopenia<br /> #Fever<br /> #Renal pathology<br /> #CNS abnormalities (seizure, AMS, CVA, coma)<br /> <br /> *TTP pentad mnemonic = FAT RN<br /> **Fever, Anemia, Thrombocytopenia, Renal, Neuro sx<br /> <br /> ==DDX==<br /> *Other microangiopathic hemolytic anemias (eg, [[HUS]], [[DIC]], [[malignant hypertension]])<br /> *[[ITP]]<br /> *[[Sepsis]]<br /> *[[SLE]]<br /> *[[HELLP]] syndrome<br /> **Difficult to distinguish<br /> **Anemia, plt count, and LDH tend to be more severe in TTP; LFTs more severe in HELLP<br /> <br /> == Work-Up ==<br /> <br /> *CBC with peripheral smear (anemia, '''schistocytes''', thrombocytopenia)<br /> *LDH (elevated)<br /> *Haptoglobin (decreased)<br /> *Reticulocyte count (appropriate)<br /> *UA (hemoglobinuria) <br /> *Creatinine (possibly elevated)<br /> *LFTs (increased bilirubin) <br /> *PT/PTT/INR (normal; differentiates from [[DIC]]) <br /> *Urine pregnancy (significant association between pregnancy and TTP)<br /> <br /> == Treatment ==<br /> <br /> *Plasma exchange (plasmapheresis) <br /> **Replaces defective or insufficient ADAMTS-13 and clears vWF multimers <br /> *Transfusion <br /> **Indicated if plasma exchange cannot be performed immediately <br /> **FFP <br /> **Platelet (only for life-threatening bleeding or intracranial hemorrhage) <br /> ***Platelet infusion may lead to acutely worsened thrombosis, renal failure, and death<br /> *Splenectomy - 2nd line therapy<br /> <br /> ==Disposition==<br /> *Admit for plasma exchange<br /> <br /> ==Source ==<br /> *Tintinalli<br /> *Harwood Nuss<br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Microangiopathic_hemolytic_anemia&diff=14058 2013-11-09T16:36:28Z

<p>Mhankerson: </p> <hr /> <div>==Introduction==<br /> '''Microangiopathic hemolytic anemia (MAHA)''' = variety of conditions that result in damaged endothelium of small vessels causing platelet aggregation and fibrin deposition which leads to shearing forces within these small vessels causing an intravascular fragmentation hemolysis<br /> <br /> <br /> ==Diagnosis==<br /> *Clinical features + heme labs<br /> *May have bleeding and thrombosis<br /> <br /> <br /> ==DDx==<br /> *Most common causes: [[DIC]], [[TTP]], [[HUS]]<br /> *Other medical causes: [[malignant hypertension]], [[HELLP]], [[antiphospholipid syndrome]], [[scleroderma]], [[PNH]], malignancy, renal allograft rejection, vasculitides like [[polyarteritis nodosa]] and [[Wegener's granulomatosis]]<br /> *Drugs: chemotherapy; [[Plavix]] (clopidogrel) associated with [[TTP]]<br /> *Nonvascular causes: prosthetic valve (more common w/ mechanical, more common at aortic valve), [[LVAD]], [[TIPS]], coil embolization, patched AV shunt, [[AVM]]<br /> <br /> ==Work-Up==<br /> *Peripheral smear, hemoglobin, platelets, PT/INR, PTT, fibrinogen, FDPs, D-dimer, haptoglobin, LDH, bilirubin<br /> **Schistocytes (aka Helmet cells) secondary to fragmentation hemolysis classic finding on peripheral smear<br /> <br /> <br /> *All MAHAs = <br /> **Schistocytes<br /> **High: +/- LDH and bili<br /> **Low: Hgb, platelets, +/- haptoglobin<br /> <br /> <br /> *DIC = '''elevated''' PT/INR/PTT/FDPs/D-dimer, '''low''' fibrinogen<br /> <br /> *TTP/HUS = '''normal''' PT/INR/PTT/FDPs/D-dimer/fibrinogen<br /> <br /> <br /> ==See Also==<br /> *[[DIC]], [[TTP]], [[HUS]]<br /> *[[Malignant hypertension]], [[HELLP]], [[antiphospholipid syndrome]], [[PNH]]<br /> *[[HIT]]<br /> <br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Microangiopathic_hemolytic_anemia&diff=14041 2013-11-09T06:27:49Z

<p>Mhankerson: edit</p> <hr /> <div>==Introduction==<br /> '''Microangiopathic hemolytic anemia (MAHA)''' = variety of conditions that result in damaged endothelium of small vessels causing platelet aggregation and fibrin deposition which leads to shearing forces within these small vessels causing an intravascular fragmentation hemolysis<br /> <br /> <br /> ==Diagnosis==<br /> *Clinical features + heme labs<br /> *May have bleeding and thrombosis<br /> <br /> <br /> ==DDx==<br /> *Most common causes: [[DIC]], [[TTP]], [[HUS]]<br /> *Other medical causes: [[malignant hypertension]], [[HELLP]], [[antiphospholipid syndrome]], [[scleroderma]], [[PNH]], malignancy, renal allograft rejection, vasculitides like [[polyarteritis nodosa]] and [[Wegener's granulomatosis]]<br /> *Drugs: chemotherapy; [[Plavix]] (clopidogrel) associated with [[TTP]]<br /> *Nonvascular causes: prosthetic valve (more common w/ mechanical, more common at aortic valve), [[LVAD]], [[TIPS]], coil embolization, patched AV shunt, [[AVM]]<br /> <br /> ==Work-Up==<br /> *Peripheral smear, hemoglobin, platelets, PT/INR, PTT, fibrinogen, FDPs, D-dimer, haptoglobin, LDH, bilirubin<br /> **Schistocytes (aka Helmet cells) secondary to fragmentation hemolysis classic finding on peripheral smear<br /> <br /> <br /> *All MAHAs = <br /> **Schistocytes<br /> **High: FDPs, D-Dimer, +/- LDH and bili<br /> **Low: Hgb, platelets, fibrinogen, +/- haptoglobin<br /> <br /> *DIC = elevated PT/INR, PTT<br /> <br /> *TTP/HUS = normal PT/INR, PTT<br /> <br /> <br /> ==See Also==<br /> *[[DIC]], [[TTP]], [[HUS]]<br /> *[[Malignant hypertension]], [[HELLP]], [[antiphospholipid syndrome]], [[PNH]]<br /> *[[HIT]]<br /> <br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Microangiopathic_hemolytic_anemia&diff=14040 2013-11-09T06:24:00Z

<p>Mhankerson: New article</p> <hr /> <div>==Introduction==<br /> '''Microangiopathic hemolytic anemia (MAHA)''' = variety of conditions that result in damaged endothelium of small vessels causing platelet aggregation and fibrin deposition which leads to shearing forces within these small vessels causing an intravascular fragmentation hemolysis<br /> <br /> <br /> ==Diagnosis==<br /> *Clinical features + heme labs<br /> *May have bleeding and thrombosis<br /> <br /> <br /> ==DDx==<br /> *Most common causes: [[DIC]], [[TTP]], [[HUS]]<br /> *Other medical causes: [[malignant hypertension]], [[HELLP]], [[antiphospholipid syndrome]], [[scleroderma]], [[PNH]], malignancy, renal allograft rejection, vasculitides like [[polyarteritis nodosa]] and [[Wegener's granulomatosis]]<br /> *Drugs: chemotherapy; Plavix (clopidogrel) associated with [[TTP]]<br /> *Nonvascular causes: prosthetic valve (more common w/ mechanical, more common at aortic valve), [[LVAD]], [[TIPS]], coil embolization, patched AV shunt, [[AVM]]<br /> <br /> <br /> ==Work-Up==<br /> *Peripheral smear, hemoglobin, platelets, PT/INR, PTT, fibrinogen, FDPs, D-dimer, haptoglobin, LDH, bilirubin<br /> **Schistocytes (aka Helmet cells) secondary to fragmentation hemolysis classic finding on peripheral smear<br /> <br /> <br /> *All MAHAs = <br /> **Schistocytes<br /> **High: FDPs, D-Dimer, +/- LDH and bili<br /> **Low: Hgb, platelets, fibrinogen, +/- haptoglobin<br /> <br /> *DIC = elevated PT/INR, PTT<br /> <br /> *TTP/HUS = normal PT/INR, PTT<br /> <br /> <br /> ==See Also==<br /> *[[DIC]], [[TTP]], [[HUS]]<br /> *[[Malignant hypertension]], [[HELLP]], [[antiphospholipid syndrome]], [[PNH]]<br /> *[[HIT]]<br /> <br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Le_Fort_fractures&diff=13605 2013-10-20T15:17:41Z

<p>Mhankerson: edit</p> <hr /> <div>==Classification==<br /> #Le Fort I<br /> ##Transverse fx separating body of maxilla from pterygoid plate and nasal septum<br /> ##Only hard palate and teeth move (when rock hard palate while stabilizing forehead)<br /> ##Stable fx<br /> #Le Fort II<br /> ##Pyramidal fx through central maxilla and hard palate<br /> ##Movement of hard palate and nose occurs, but not the eyes<br /> ##Can be stable or unstable fx<br /> #Le Fort III<br /> ##Craniofacial dysjunction (fx through frontozygomatic sutures, orbit, nose, ethmoids)<br /> ##Entire face shifts w/ globes held in place only by optic nerve)<br /> ##Unstable fx<br /> <br /> ==Management==<br /> *Airway protection<br /> **Consider awake intubation (eg, ketamine) if need airway; if possible do not paralyze a Le Fort for intubation or you may be forced into a crash surgical airway<br /> **Prepare for surgical airway<br /> *CT Face<br /> *Control hemorrhage w/ nasal and oral packing if needed<br /> *Admit for IV abx and sx<br /> <br /> ==See Also==<br /> *[[Maxillofacial Trauma]]<br /> <br /> ==Source==<br /> Tintinalli<br /> <br /> [[Category:ENT]]<br /> [[Category:Ortho]]<br /> [[Category:Trauma]]</div>

Mhankerson https://wikem.org/w/index.php?title=Left_ventricular_aneurysm&diff=13603 2013-10-18T19:35:11Z

<p>Mhankerson: edit</p> <hr /> <div>==Introduction==<br /> LV Aneurysm = thin/fibrotic wall with no/necrotic muscle that is akinetic or dyskinetic (paradoxical ballooning)<br /> <br /> ==Causes==<br /> *Majority: healed transmural MI (anterior most common)<br /> *Rare: HOCM, Chagas<br /> <br /> ==Diagnosis==<br /> *Can be asymptomatic<br /> *Hx of MI<br /> *Angina, SOB/DOE, CHF sx<br /> *Mitral regurg murmur, S3/S4<br /> *EKG: persistent characteristic ST elevation after MI <br /> *CXR: prominent left heart border, calcified aneurysm<br /> *TTE, LV angiography, cardiac MRI<br /> <br /> ==Complications==<br /> *Heart failure (LV aneurysm steals CO)<br /> *Angina (increased O2 demand)<br /> *Ventricular arrhythmias (LV stretch/scarring)<br /> *LV thrombus (50% of time), arterial embolism (stroke)<br /> *LV rupture (rarely occurs in mature LVA because of dense fibrosis)<br /> <br /> ==Medical Therapy (first line)==<br /> *Afterload reduction (ACEI)<br /> *Antianginal (Nitro)<br /> *Anticoagulation (if LV thrombus)<br /> <br /> ==Surgical Therapy==<br /> *Aneurysmectomy and CABG (and possible valve repair) if ventricular arrhythmias and/or HF refractory to medical therapy<br /> <br /> ==See Also==<br /> *[[Left Ventricular Pseudoaneurysm]]<br /> <br /> [[Category:Cards]]</div>

Mhankerson https://wikem.org/w/index.php?title=Left_ventricular_pseudoaneurysm&diff=13602 2013-10-18T19:34:03Z

<p>Mhankerson: new article</p> <hr /> <div>==Introduction==<br /> *LV Pseudoaneurysm = acute MI causes ventricular free wall rupture that is contained by pericardial adhesions<br /> **Only small ones compatible with life<br /> <br /> ==Causes==<br /> *Transmural MI (anterior most common)<br /> <br /> ==Diagnosis==<br /> *Can be asymptomatic<br /> *Hx of MI<br /> *Angina, SOB/DOE<br /> *LV angiography (TTE unreliable)<br /> <br /> ==Complications==<br /> *Angina (increased O2 demand)<br /> *Complete LV rupture<br /> <br /> ==Treatment==<br /> *Surgical repair = 10% 5 yr mortality<br /> *Medical therapy = 50% 5 yr mortality<br /> <br /> ==See Also==<br /> *[[Left Ventricular Aneurysm]]<br /> <br /> [[Category:Cards]]</div>

Mhankerson https://wikem.org/w/index.php?title=Left_ventricular_aneurysm&diff=13601 2013-10-18T19:26:42Z

<p>Mhankerson: new article</p> <hr /> <div>==Introduction==<br /> LV Aneurysm = thin/fibrotic wall with no/necrotic muscle that is akinetic or dyskinetic (paradoxical ballooning)<br /> <br /> ==Causes==<br /> *Majority: healed transmural MI (anterior most common)<br /> *Rare: HOCM, Chagas<br /> <br /> ==Diagnosis==<br /> *Can be asymptomatic<br /> *Hx of MI<br /> *Mitral regurg murmur, S3/S4<br /> *EKG: persistent characteristic ST elevation after MI <br /> *CXR: prominent left heart border, calcified aneurysm<br /> *TTE, LV angiography, cardiac MRI<br /> <br /> ==Complications==<br /> *Heart failure (LV aneurysm steals CO)<br /> *Angina (increased O2 demand)<br /> *Ventricular arrhythmias (LV stretch/scarring)<br /> *LV thrombus (50% of time), arterial embolism (stroke)<br /> *LV rupture (rarely occurs in mature LVA because of dense fibrosis)<br /> <br /> ==Medical Therapy (first line)==<br /> *Afterload reduction (ACEI)<br /> *Antianginal (Nitro)<br /> *Anticoagulation (if LV thrombus)<br /> <br /> ==Surgical Therapy==<br /> *Aneurysmectomy and CABG (and possible valve repair) if ventricular arrhythmias and/or HF refractory to medical therapy<br /> <br /> ==See Also==<br /> *[[Left Ventricular Pseudoaneurysm]]<br /> <br /> [[Category:Cards]]</div>

Mhankerson https://wikem.org/w/index.php?title=T_Wave_Inversions&diff=13567 2013-10-11T03:13:37Z

<p>Mhankerson: minor edit</p> <hr /> <div>DDX<br /> #Myocardial infarct (NSTEMI)<br /> #Myocardial ischemia (Wellen's)<br /> #Pulmonary embolism (RV strain)<br /> #LVH with strain pattern<br /> #Bundle branch block<br /> #Pericarditis (stage 3)<br /> #CNS T waves (diffuse, deep)<br /> #ARVD (may also have epsilon wave)<br /> <br /> [[Category:Cards]]</div>

Mhankerson https://wikem.org/w/index.php?title=T_Wave_Inversions&diff=13566 2013-10-11T03:08:05Z

<p>Mhankerson: new article</p> <hr /> <div>DDX<br /> #Myocardial infarct (NSTEMI)<br /> #Myocardial ischemia (Wellen's)<br /> #Pulmonary embolism (RV strain)<br /> #LVH with strain pattern<br /> #Bundle branch block<br /> #Pericarditis (stage 3)<br /> #CNS T waves<br /> <br /> [[Category:Cards]]</div>

Mhankerson https://wikem.org/w/index.php?title=Peaked_T_waves&diff=13565 2013-10-11T02:55:55Z

<p>Mhankerson: new article</p> <hr /> <div>DDx<br /> #MI (hyperacute T waves)<br /> #Hyperkalemia<br /> #Benign Early Repolarization<br /> <br /> [[Category:Cards]]</div>

Mhankerson https://wikem.org/w/index.php?title=ST_segment_elevation&diff=13564 2013-10-11T02:36:07Z

<p>Mhankerson: Edited, minor additions and reformatting</p> <hr /> <div>==Background==<br /> *Its presence must be explained (there is no &quot;nonspecific ST elevation&quot;)<br /> *Not a specific marker for STEMI<br /> <br /> ==DDX==<br /> #Myocardial Infarct ([[STEMI]])<br /> #[[Wellens' Syndrome]]<br /> #Coronary spasm (eg, Prinzmetal's angina)<br /> #Drugs (eg, cocaine, crack, meth)<br /> #[[Pericarditis]]<br /> #LV aneurysm<br /> #Early repolarization<br /> #LBBB<br /> #LVH<br /> #Misc<br /> ##Meds: TCA, digoxin<br /> ##RV pacing (appears as LBBB)<br /> ##Hyperkalemia<br /> ##Hypothermia<br /> ###&quot;Osborn J waves&quot;<br /> ##[[Brugada Syndrome]]<br /> <br /> ==Early Repolarization versus STEMI==<br /> *Early Repolarization suggested by:<br /> **ST elevation &lt;4mm<br /> **Notched J point<br /> **Concave or saddle-back ST morphology<br /> **No reciprocal changes<br /> <br /> ==LVH versus STEMI==<br /> *Difficult to exclude MI in pt with LVH (pt already at risk for MI)<br /> *Best aid is prior ECG or serial ECGs<br /> <br /> ==LBBB versus STEMI==<br /> See [[Sgarbossa's Criteria]]<br /> <br /> ==STEMI==<br /> *ST elevation in those leads that reflect the distribution of a single coronary artery<br /> **RCA: II, III, aVF (inferior)<br /> **LAD: V1-V4 (antero-septal)<br /> **Circumflex: V5-V6, I, aVL (lateral)<br /> **Dominant left circulation: infero-lateral<br /> *ST morphology<br /> **Concave up versus convex<br /> ***Convex has Sp 97%, Sn 77%<br /> *Look for reciprocal ST depression<br /> **35% of anterior STEMI have ST depression in inferior leads<br /> **80% of inferior STEMI have ST depression in anterior leads<br /> ***However, may represent reciprocal changes OR posterior STEMI<br /> <br /> ==Source==<br /> *ST Elevation Lecture, Dr. Niemann, Harbor-UCLA<br /> <br /> [[Category:Cards]]</div>

Mhankerson https://wikem.org/w/index.php?title=Wide_QRS&diff=13563 2013-10-11T01:56:07Z

<p>Mhankerson: new article</p> <hr /> <div>DDx<br /> #Ventricular rhythm<br /> #MI<br /> #Bundle branch block<br /> #Hyperkalemia<br /> #Drugs (eg, TCAs, digoxin, antiarrhythmics)<br /> #Paced rhythm<br /> #Myocarditis<br /> #WPW (delta wave, antidromic)<br /> #ARVD (epsilon wave)<br /> <br /> <br /> [[Category:Cards]]</div>

Mhankerson https://wikem.org/w/index.php?title=ST_segment_depression&diff=13562 2013-10-11T00:37:18Z

<p>Mhankerson: </p> <hr /> <div>==DDX==<br /> #Posterior MI<br /> #RV strain<br /> #NSTEMI<br /> #Reciprocal changes<br /> #Electrolyte disorder (e.g. hypokalemia)<br /> #LVH with strain pattern (repolarization abnormality)<br /> #Digoxin effect (not indicative of toxicity)<br /> <br /> ==Source==<br /> ST Elevation Lecture, Dr. Niemann, Harbor-UCLA<br /> <br /> [[Category:Cards]]</div>

Mhankerson https://wikem.org/w/index.php?title=ST_segment_depression&diff=13561 2013-10-11T00:28:08Z

<p>Mhankerson: </p> <hr /> <div>==DDX==<br /> #Posterior MI<br /> #RV strain<br /> #Anterior NSTEMI<br /> #Reciprocal changes<br /> #Electrolyte disorder (e.g. hypokalemia)<br /> #LVH with strain pattern (repolarization abnormality)<br /> #Digoxin use<br /> <br /> ==Source==<br /> ST Elevation Lecture, Dr. Niemann, Harbor-UCLA<br /> <br /> [[Category:Cards]]</div>

Mhankerson https://wikem.org/w/index.php?title=Thrombotic_thrombocytopenic_purpura&diff=13502 2013-10-04T17:46:01Z

<p>Mhankerson: </p> <hr /> <div>==Background==<br /> *Pathophysiology<br /> **Insufficient ADAMTS-13 activity allows vWF multimers to accumulate in microcirculation<br /> ***Leads to platelet aggregation/thrombocytopenia and hemolysis of RBCs<br /> *Similar to but different from [[HUS]] (which is more common in peds)<br /> *Microangiopathic hemolytic anemia + low plts is TTP until proven otherwise<br /> <br /> ===Risk Factors===<br /> *Congenitally deficient ADAMTS-13 activity and:<br /> #Pregnancy<br /> #Infection<br /> #Inflammation<br /> #Medication use (quinolones, ticlopidine, clopidogrel)<br /> <br /> ==Clinical Features==<br /> *Pentad<br /> #Microangiopathic hemolytic anemia<br /> #Thrombocytopenia<br /> #Fever<br /> #Renal pathology<br /> #CNS abnormalities (seizure, AMS, CVA, coma)<br /> <br /> *TTP pentad mnemonic = FAT RN<br /> **Fever, Anemia, Thrombocytopenia, Renal, Neuro sx<br /> <br /> ==DDX==<br /> *Other microangiopathic hemolytic anemias (HUS, DIC, malignant HTN)<br /> *ITP<br /> *Sepsis<br /> *SLE<br /> *HELLP syndrome<br /> **Difficult to distinguish<br /> **Anemia, plt count, and LDH tend to be more severe in TTP; LFTs more severe in HELLP<br /> <br /> == Work-Up ==<br /> <br /> *CBC with peripheral smear (anemia, '''schistocytes''', thrombocytopenia)<br /> *LDH (elevated)<br /> *Haptoglobin (decreased)<br /> *Reticulocyte count (appropriate)<br /> *UA (hemoglobinuria) <br /> *Creatinine (possibly elevated)<br /> *LFTs (increased bilirubin) <br /> *PT/PTT/INR (normal; differentiates from DIC) <br /> *Urine pregnancy (significant association between pregnancy and TTP)<br /> <br /> == Treatment ==<br /> <br /> *Plasma exchange (plasmapheresis) <br /> **Replaces defective or insufficient ADAMTS-13 and clears vWF multimers <br /> *Transfusion <br /> **Indicated if plasma exchange cannot be performed immediately <br /> **FFP <br /> **Platelet (only for life-threatening bleeding or intracranial hemorrhage) <br /> ***Platelet infusion may lead to acutely worsened thrombosis, renal failure, and death<br /> *Splenectomy - 2nd line therapy<br /> <br /> ==Disposition==<br /> *Admit for plasma exchange<br /> <br /> ==Source ==<br /> *Tintinalli<br /> *Harwood Nuss<br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Thrombotic_thrombocytopenic_purpura&diff=13501 2013-10-04T17:31:59Z

<p>Mhankerson: </p> <hr /> <div>==Background==<br /> *Pathophysiology<br /> **Insufficient ADAMTS-13 activity allows vWF multimers to accumulate in microcirculation<br /> ***Leads to platelet aggregation/thrombocytopenia and hemolysis of RBCs<br /> *Similar to but different from [[HUS]] (which is more common in peds)<br /> *Microangiopathic hemolytic anemia + low plts is TTP until proven otherwise<br /> <br /> ===Risk Factors===<br /> #Congenitally deficient ADAMTS-13 activity and:<br /> ##Pregnancy<br /> ##Infection<br /> ##Inflammation<br /> ##Medication use<br /> ###Quinolones, ticlopidine, clopidogrel<br /> <br /> ==Clinical Features==<br /> #Pentad<br /> ##CNS abnormalities<br /> ###Seizure, CVA, coma<br /> ##Renal pathology<br /> ##Microangiopathic hemolytic anemia<br /> ##Thrombocytopenia<br /> ##Fever<br /> <br /> #TTP pentad mnemonic = FAT RN<br /> ##Fever, Anemia, Thrombocytopenia, Renal, Neuro sx<br /> <br /> ==DDX==<br /> #Other microangiopathic hemolytic anemias (HUS, DIC, malignant HTN)<br /> #ITP<br /> #Sepsis<br /> #SLE<br /> #HELLP syndrome<br /> ##Difficult to distinguish<br /> ##Anemia, plt count, and LDH tend to be more severe in TTP; LFTs more severe in HELLP<br /> <br /> == Work-Up ==<br /> <br /> #CBC with peripheral smear<br /> ##Anemia, '''schistocytes''', thrombocytopenia <br /> #LDH <br /> #Haptoglobin <br /> #UA <br /> ##Hemoglobinuria <br /> ##Creatinine <br /> #LFT <br /> ##Increased bilirubin <br /> #PT/PTT/INR <br /> ##Normal (differentiates from DIC) <br /> #Urine pregnancy <br /> ##Significant association between pregnancy and TTP<br /> <br /> == Treatment ==<br /> <br /> #Plasma exchange (plasmapheresis) <br /> ##Replaces defective or insufficient ADAMTS-13 and clears vWF multimers <br /> #Transfusion <br /> ##Indicated if plasma exchange cannot be performed immediately <br /> ##FFP <br /> ##Platelet (only for life-threatening bleeding or intracranial hemorrhage) <br /> ###Platelet infusion may lead to acutely worsened thrombosis, renal failure, and death<br /> #Splenectomy - 2nd line therapy<br /> <br /> ==Disposition==<br /> *Admit for plasma exchange<br /> <br /> ==Source ==<br /> *Tintinalli<br /> *Harwood Nuss<br /> [[Category:Heme/Onc]]</div>

Mhankerson https://wikem.org/w/index.php?title=Thiamine_deficiency&diff=13139 2013-09-25T15:45:42Z

<p>Mhankerson: </p> <hr /> <div>==See Also==<br /> *[[Wernicke's Encephalopathy]]<br /> *[[Korsakoff's Psychosis]]<br /> *[[Wernicke-Korsakoff Syndrome]]<br /> *[[Beriberi]]<br /> <br /> [[Category:Neuro]]</div>

Mhankerson https://wikem.org/w/index.php?title=Beriberi&diff=13138 2013-09-25T15:44:34Z

<p>Mhankerson: </p> <hr /> <div>==Background==<br /> *Dry Beriberi: neuro sx caused by thiamine deficiency<br /> *Wet Beriberi: cardiac sx caused by thiamine deficiency<br /> *Infantile Beriberi: neuro/cardiac sx caused by thiamine deficiency in &lt;1 year old infant<br /> <br /> ==Causes==<br /> *Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement<br /> **Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis<br /> <br /> ==Diagnosis==<br /> Beriberi = clinical diagnosis<br /> <br /> <br /> Dry Beriberi<br /> *Sx: symmetrical peripheral neuropathy (motor and sensory) mostly distal extremities<br /> <br /> <br /> Wet Beriberi<br /> *Sx: CHF, high output heart failure, cardiomegaly, peripheral edema, tachycardia, DOE/PND/orthopnea<br /> *Can include neuropathy seen in Dry Beriberi<br /> <br /> <br /> Infantile Beriberi<br /> *Sx: CHF, cardiomegaly, tachycardia, cyanosis, dyspnea, weight loss, marasmus, vomiting, loud cry, nystagmus, seizure<br /> <br /> ==Treatment==<br /> Thiamine 50-100 mg IV/IM q day x 7-14 days, then 10 mg PO q day until complete recovery<br /> <br /> <br /> *If you suspect Beriberi then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high<br /> <br /> *Remember to give magnesium; hypomagnesemic state may be resistant to thiamine administration<br /> <br /> *Give multivitamin since pt at risk for other vitamin deficiencies <br /> <br /> *For chronic alcoholics always consider banana bag: thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W<br /> <br /> *Remember to give thiamine BEFORE glucose in pts requiring glucose who are at risk for thiamine deficiency; glucose without thiamine can precipitate/worsen WE by driving thiamine intracellularly<br /> <br /> ==See Also==<br /> *[[Wernicke's Encephalopathy]]<br /> *[[Korsakoff's Psychosis]]<br /> *[[Wernicke-Korsakoff Syndrome]]<br /> *[[Thiamine deficiency]]<br /> <br /> [[Category:Neuro]]<br /> [[Category:Cards]]</div>

Mhankerson https://wikem.org/w/index.php?title=Wernicke-Korsakoff_syndrome&diff=13137 2013-09-25T15:43:48Z

<p>Mhankerson: </p> <hr /> <div>==Background==<br /> *Wernicke’s Encephalopathy (WE): ACUTE neuro/cardiovascular sx caused by thiamine deficiency<br /> *Korsakoff’s Psychosis (KP): CHRONIC neurologic symptoms caused by thiamine deficiency<br /> *Wernicke-Korsakoff Syndrome (WKS): presence of WE + KP simultaneously<br /> <br /> ==Epidemiology==<br /> *Only 20% identified before death, failure of dx leads to 20% mortality and 75% permanent damage<br /> <br /> ==Causes==<br /> *Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement<br /> **Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis<br /> <br /> ==Pathophysiology==<br /> *Brain lesions/atrophy occurs: mamillary bodies (nearly all cases), thalamus, periaqueductal gray matter, 3rd/4th ventricle, cerebellum, frontal lobe<br /> <br /> ==Diagnosis==<br /> WE/KP/WKS = clinical diagnoses<br /> <br /> ===Wernicke’s Encephalopathy===<br /> *Classic triad: encephalopathy, oculomotor dysfunction, gait ataxia<br /> *werNICke mnemonic: <br /> **N: Nystagmus/ophthalmoplegia<br /> **I: Incoordination/ataxia<br /> **C: Confusion/memory impairment<br /> *Other sx: hypotension, tachycardia, EKG abnormalities, DOE, CHF sx, hypothermia, coma, dry/wet Beriberi<br /> <br /> ===Korsakoff’s Psychosis===<br /> *Sx: anterograde/retrograde amnesia, confabulation, confusion, apathy<br /> <br /> ===Wernicke-Korsakoff Syndrome===<br /> *Sx: combination of WE and KP<br /> <br /> ==Treatment==<br /> If suspect WE/KP/WKS: thiamine 500 mg IV over 30 min TID x 2 days, then 500 mg IV/IM q day for 5 days, then 100 mg PO q day until pt no longer at risk<br /> <br /> <br /> If suspect at risk for thiamine deficiency but no sx: thiamine 100 mg PO q day<br /> <br /> <br /> *If you suspect WE/KP/WKS then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high<br /> <br /> *Give magnesium; hypomagnesemic state may be resistant to thiamine administration<br /> <br /> *Give multivitamin; pt at risk for other vitamin deficiencies <br /> <br /> *For chronic alcoholics always consider banana bag: thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W<br /> <br /> *Remember to give thiamine BEFORE glucose in pts requiring glucose who are at risk for thiamine deficiency; glucose without thiamine can precipitate/worsen WE by driving thiamine intracellularly<br /> <br /> ==See Also==<br /> *[[Beriberi]]<br /> *[[Thiamine deficiency]]<br /> <br /> [[Category:Neuro]]</div>

Mhankerson https://wikem.org/w/index.php?title=Wernicke-Korsakoff_syndrome&diff=12961 2013-09-20T15:47:21Z

<p>Mhankerson: </p> <hr /> <div>==Background==<br /> *Wernicke’s Encephalopathy (WE): ACUTE neuro/cardiovascular sx caused by thiamine deficiency<br /> *Korsakoff’s Psychosis (KP): CHRONIC neuro sx caused by thiamine deficiency<br /> *Wernicke-Korsakoff Syndrome (WKS): presence of WE + KP simultaneously <br /> <br /> ==Epidemiology==<br /> *Only 20% identified before death, failure of dx leads to 20% mortality and 75% permanent damage<br /> <br /> ==Causes==<br /> *Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement<br /> **Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis<br /> <br /> ==Pathophysiology==<br /> *Brain lesions/atrophy occurs: mamillary bodies (nearly all cases), thalamus, periaqueductal gray matter, 3rd/4th ventricle, cerebellum, frontal lobe<br /> <br /> ==Diagnosis==<br /> WE/KP/WKS = clinical diagnoses<br /> <br /> <br /> Wernicke’s Encephalopathy<br /> *Classic triad: encephalopathy, oculomotor dysfunction, gait ataxia<br /> *werNICke mnemonic: <br /> **N: Nystagmus/ophthalmoplegia<br /> **I: Incoordination/ataxia<br /> **C: Confusion/memory impairment<br /> *Other sx: hypotension, tachycardia, EKG abnormalities, DOE, CHF sx, hypothermia, coma, dry/wet Beriberi<br /> <br /> <br /> Korsakoff’s Psychosis<br /> *Sx: anterograde/retrograde amnesia, confabulation, confusion, apathy<br /> <br /> <br /> Wernicke-Korsakoff Syndrome<br /> *Sx: combination of WE and KP<br /> <br /> ==Treatment==<br /> If suspect WE/KP/WKS: thiamine 500 mg IV over 30 min TID x 2 days, then 500 mg IV/IM q day for 5 days, then 100 mg PO q day until pt no longer at risk<br /> <br /> <br /> If suspect at risk for thiamine deficiency but no sx: thiamine 100 mg PO q day<br /> <br /> <br /> *If you suspect WE/KP/WKS then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high<br /> <br /> *Give magnesium; hypomagnesemic state may be resistant to thiamine administration<br /> <br /> *Give multivitamin; pt at risk for other vitamin deficiencies <br /> <br /> *For chronic alcoholics always consider banana bag: thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W<br /> <br /> *Remember to give thiamine BEFORE glucose in pts requiring glucose who are at risk for thiamine deficiency; glucose without thiamine can precipitate/worsen WE by driving thiamine intracellularly<br /> <br /> ==See Also==<br /> *[[Wernicke's Encephalopathy]]<br /> *[[Korsakoff's Psychosis]]<br /> *[[Beriberi]]<br /> *[[Thiamine deficiency]]</div>

Mhankerson https://wikem.org/w/index.php?title=Korsakoff%27s_Psychosis&diff=12960 2013-09-20T15:46:44Z

<p>Mhankerson: </p> <hr /> <div>==Background==<br /> *Wernicke’s Encephalopathy (WE): ACUTE neuro/cardiovascular sx caused by thiamine deficiency<br /> *Korsakoff’s Psychosis (KP): CHRONIC neuro sx caused by thiamine deficiency<br /> *Wernicke-Korsakoff Syndrome (WKS): presence of WE + KP simultaneously <br /> <br /> ==Epidemiology==<br /> *Only 20% identified before death, failure of dx leads to 20% mortality and 75% permanent damage<br /> <br /> ==Causes==<br /> *Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement<br /> **Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis<br /> <br /> ==Pathophysiology==<br /> *Brain lesions/atrophy occurs: mamillary bodies (nearly all cases), thalamus, periaqueductal gray matter, 3rd/4th ventricle, cerebellum, frontal lobe<br /> <br /> ==Diagnosis==<br /> WE/KP/WKS = clinical diagnoses<br /> <br /> <br /> Wernicke’s Encephalopathy<br /> *Classic triad: encephalopathy, oculomotor dysfunction, gait ataxia<br /> *werNICke mnemonic: <br /> **N: Nystagmus/ophthalmoplegia<br /> **I: Incoordination/ataxia<br /> **C: Confusion/memory impairment<br /> *Other sx: hypotension, tachycardia, EKG abnormalities, DOE, CHF sx, hypothermia, coma, dry/wet Beriberi<br /> <br /> <br /> Korsakoff’s Psychosis<br /> *Sx: anterograde/retrograde amnesia, confabulation, confusion, apathy<br /> <br /> <br /> Wernicke-Korsakoff Syndrome<br /> *Sx: combination of WE and KP<br /> <br /> ==Treatment==<br /> If suspect WE/KP/WKS: thiamine 500 mg IV over 30 min TID x 2 days, then 500 mg IV/IM q day for 5 days, then 100 mg PO q day until pt no longer at risk<br /> <br /> <br /> If suspect at risk for thiamine deficiency but no sx: thiamine 100 mg PO q day<br /> <br /> <br /> *If you suspect WE/KP/WKS then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high<br /> <br /> *Give magnesium; hypomagnesemic state may be resistant to thiamine administration<br /> <br /> *Give multivitamin; pt at risk for other vitamin deficiencies <br /> <br /> *For chronic alcoholics always consider banana bag: thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W<br /> <br /> *Remember to give thiamine BEFORE glucose in pts requiring glucose who are at risk for thiamine deficiency; glucose without thiamine can precipitate/worsen WE by driving thiamine intracellularly<br /> <br /> ==See Also==<br /> *[[Wernicke's Encephalopathy]]<br /> *[[Wernicke-Korsakoff Syndrome]]<br /> *[[Beriberi]]<br /> *[[Thiamine deficiency]]</div>

Mhankerson https://wikem.org/w/index.php?title=Wernicke%27s_Encephalopathy&diff=12959 2013-09-20T15:46:10Z

<p>Mhankerson: </p> <hr /> <div>==Background==<br /> *Wernicke’s Encephalopathy (WE): ACUTE neuro/cardiovascular sx caused by thiamine deficiency<br /> *Korsakoff’s Psychosis (KP): CHRONIC neuro sx caused by thiamine deficiency<br /> *Wernicke-Korsakoff Syndrome (WKS): presence of WE + KP simultaneously <br /> <br /> ==Epidemiology==<br /> *Only 20% identified before death, failure of dx leads to 20% mortality and 75% permanent damage<br /> <br /> ==Causes==<br /> *Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement<br /> **Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis<br /> <br /> ==Pathophysiology==<br /> *Brain lesions/atrophy occurs: mamillary bodies (nearly all cases), thalamus, periaqueductal gray matter, 3rd/4th ventricle, cerebellum, frontal lobe<br /> <br /> ==Diagnosis==<br /> WE/KP/WKS = clinical diagnoses<br /> <br /> <br /> Wernicke’s Encephalopathy<br /> *Classic triad: encephalopathy, oculomotor dysfunction, gait ataxia<br /> *werNICke mnemonic: <br /> **N: Nystagmus/ophthalmoplegia<br /> **I: Incoordination/ataxia<br /> **C: Confusion/memory impairment<br /> *Other sx: hypotension, tachycardia, EKG abnormalities, DOE, CHF sx, hypothermia, coma, dry/wet Beriberi<br /> <br /> <br /> Korsakoff’s Psychosis<br /> *Sx: anterograde/retrograde amnesia, confabulation, confusion, apathy<br /> <br /> <br /> Wernicke-Korsakoff Syndrome<br /> *Sx: combination of WE and KP<br /> <br /> ==Treatment==<br /> If suspect WE/KP/WKS: thiamine 500 mg IV over 30 min TID x 2 days, then 500 mg IV/IM q day for 5 days, then 100 mg PO q day until pt no longer at risk<br /> <br /> <br /> If suspect at risk for thiamine deficiency but no sx: thiamine 100 mg PO q day<br /> <br /> <br /> *If you suspect WE/KP/WKS then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high<br /> <br /> *Give magnesium; hypomagnesemic state may be resistant to thiamine administration<br /> <br /> *Give multivitamin; pt at risk for other vitamin deficiencies <br /> <br /> *For chronic alcoholics always consider banana bag: thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W<br /> <br /> *Remember to give thiamine BEFORE glucose in pts requiring glucose who are at risk for thiamine deficiency; glucose without thiamine can precipitate/worsen WE by driving thiamine intracellularly<br /> <br /> ==See Also==<br /> *[[Korsakoff's Psychosis]]<br /> *[[Wernicke-Korsakoff Syndrome]]<br /> *[[Beriberi]]<br /> *[[Thiamine deficiency]]</div>

Mhankerson https://wikem.org/w/index.php?title=User:Mhankerson&diff=12958 2013-09-20T15:39:00Z

<p>Mhankerson: </p> <hr /> <div>Matthew Hankerson, MD<br /> <br /> Emergency Medicine, PGY2<br /> <br /> LAC+USC Medical Center<br /> <br /> matthewhankerson@gmail.com</div>

Mhankerson https://wikem.org/w/index.php?title=User:Mhankerson&diff=12957 2013-09-20T15:38:32Z

<p>Mhankerson: Created page with &quot;Matthew Hankerson, MD Emergency Medicine, PGY2 LAC+USC Medical Center matthewhankerson@gmail.com&quot;</p> <hr /> <div>Matthew Hankerson, MD<br /> Emergency Medicine, PGY2<br /> LAC+USC Medical Center<br /> matthewhankerson@gmail.com</div>

Mhankerson https://wikem.org/w/index.php?title=Beriberi&diff=12955 2013-09-19T16:15:09Z

<p>Mhankerson: new note</p> <hr /> <div>==Background==<br /> *Dry Beriberi: neuro sx caused by thiamine deficiency<br /> *Wet Beriberi: cardiac sx caused by thiamine deficiency<br /> *Infantile Beriberi: neuro/cardiac sx caused by thiamine deficiency in &lt;1 year old infant<br /> <br /> ==Causes==<br /> *Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement<br /> **Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis<br /> <br /> ==Diagnosis==<br /> Beriberi = clinical diagnosis<br /> <br /> <br /> Dry Beriberi<br /> *Sx: symmetrical peripheral neuropathy (motor and sensory) mostly distal extremities<br /> <br /> <br /> Wet Beriberi<br /> *Sx: CHF, high output heart failure, cardiomegaly, peripheral edema, tachycardia, DOE/PND/orthopnea<br /> *Can include neuropathy seen in Dry Beriberi<br /> <br /> <br /> Infantile Beriberi<br /> *Sx: CHF, cardiomegaly, tachycardia, cyanosis, dyspnea, weight loss, marasmus, vomiting, loud cry, nystagmus, seizure<br /> <br /> ==Treatment==<br /> Thiamine 50-100 mg IV/IM q day x 7-14 days, then 10 mg PO q day until complete recovery<br /> <br /> <br /> *If you suspect Beriberi then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high<br /> <br /> *Remember to give magnesium; hypomagnesemic state may be resistant to thiamine administration<br /> <br /> *Give multivitamin since pt at risk for other vitamin deficiencies <br /> <br /> *For chronic alcoholics always consider banana bag: thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W<br /> <br /> *Remember to give thiamine BEFORE glucose in pts requiring glucose who are at risk for thiamine deficiency; glucose without thiamine can precipitate/worsen WE by driving thiamine intracellularly<br /> <br /> ==See Also==<br /> *[[Wernicke's Encephalopathy]]<br /> *[[Korsakoff's Psychosis]]<br /> *[[Wernicke-Korsakoff Syndrome]]<br /> *[[Thiamine deficiency]]</div>

Mhankerson https://wikem.org/w/index.php?title=Thiamine_deficiency&diff=12954 2013-09-19T15:31:08Z

<p>Mhankerson: new note</p> <hr /> <div>==See Also==<br /> *[[Wernicke's Encephalopathy]]<br /> *[[Korsakoff's Psychosis]]<br /> *[[Wernicke-Korsakoff Syndrome]]<br /> *[[Beriberi]]</div>

Mhankerson https://wikem.org/w/index.php?title=Wernicke%27s_Encephalopathy&diff=12953 2013-09-19T15:27:06Z

<p>Mhankerson: minor edit</p> <hr /> <div>==Background==<br /> *Wernicke’s Encephalopathy (WE): ACUTE neuro/cardiovascular sx caused by thiamine deficiency<br /> *Korsakoff’s Psychosis (KP): CHRONIC neuro sx caused by thiamine deficiency<br /> *Wernicke-Korsakoff Syndrome (WKS): presence of WE + KP simultaneously <br /> <br /> ==Epidemiology==<br /> *Only 20% identified before death, failure of dx leads to 20% mortality and 75% permanent damage<br /> <br /> ==Causes==<br /> *Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement<br /> **Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis<br /> <br /> ==Pathophysiology==<br /> *Brain lesions/atrophy occurs: mamillary bodies (nearly all cases), thalamus, periaqueductal gray matter, 3rd/4th ventricle, cerebellum, frontal lobe<br /> <br /> ==Diagnosis==<br /> WE/KP/WKS = clinical diagnoses<br /> <br /> <br /> Wernicke’s Encephalopathy<br /> *Classic triad: encephalopathy, oculomotor dysfunction, gait ataxia<br /> *werNICke mnemonic: <br /> **N: Nystagmus/ophthalmoplegia<br /> **I: Incoordination/ataxia<br /> **C: Confusion/memory impairment<br /> *Other sx: hypotension, tachycardia, EKG abnormalities, DOE, CHF sx, hypothermia, coma, dry/wet Beriberi<br /> <br /> <br /> Korsakoff’s Psychosis<br /> *Sx: anterograde/retrograde amnesia, confabulation, confusion, apathy<br /> <br /> <br /> Wernicke-Korsakoff Syndrome<br /> *Sx: combination of WE and KP<br /> <br /> ==Treatment==<br /> If suspect WE/KP/WKS: thiamine 500 mg IV over 30 min TID x 2 days, then 500 mg IV/IM q day for 5 days, then 100 mg PO q day until pt no longer at risk<br /> <br /> <br /> If suspect at risk for thiamine deficiency but no sx: thiamine 100 mg PO q day<br /> <br /> <br /> *If you suspect WE/KP/WKS then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high<br /> <br /> *Give magnesium; hypomagnesemic state may be resistant to thiamine administration<br /> <br /> *Give multivitamin; pt at risk for other vitamin deficiencies <br /> <br /> *For chronic alcoholics always consider banana bag: thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W<br /> <br /> ==See Also==<br /> *[[Korsakoff's Psychosis]]<br /> *[[Wernicke-Korsakoff Syndrome]]<br /> *[[Beriberi]]<br /> *[[Thiamine deficiency]]</div>

Mhankerson https://wikem.org/w/index.php?title=Korsakoff%27s_Psychosis&diff=12952 2013-09-19T15:26:36Z

<p>Mhankerson: minor edit</p> <hr /> <div>==Background==<br /> *Wernicke’s Encephalopathy (WE): ACUTE neuro/cardiovascular sx caused by thiamine deficiency<br /> *Korsakoff’s Psychosis (KP): CHRONIC neuro sx caused by thiamine deficiency<br /> *Wernicke-Korsakoff Syndrome (WKS): presence of WE + KP simultaneously <br /> <br /> ==Epidemiology==<br /> *Only 20% identified before death, failure of dx leads to 20% mortality and 75% permanent damage<br /> <br /> ==Causes==<br /> *Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement<br /> **Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis<br /> <br /> ==Pathophysiology==<br /> *Brain lesions/atrophy occurs: mamillary bodies (nearly all cases), thalamus, periaqueductal gray matter, 3rd/4th ventricle, cerebellum, frontal lobe<br /> <br /> ==Diagnosis==<br /> WE/KP/WKS = clinical diagnoses<br /> <br /> <br /> Wernicke’s Encephalopathy<br /> *Classic triad: encephalopathy, oculomotor dysfunction, gait ataxia<br /> *werNICke mnemonic: <br /> **N: Nystagmus/ophthalmoplegia<br /> **I: Incoordination/ataxia<br /> **C: Confusion/memory impairment<br /> *Other sx: hypotension, tachycardia, EKG abnormalities, DOE, CHF sx, hypothermia, coma, dry/wet Beriberi<br /> <br /> <br /> Korsakoff’s Psychosis<br /> *Sx: anterograde/retrograde amnesia, confabulation, confusion, apathy<br /> <br /> <br /> Wernicke-Korsakoff Syndrome<br /> *Sx: combination of WE and KP<br /> <br /> ==Treatment==<br /> If suspect WE/KP/WKS: thiamine 500 mg IV over 30 min TID x 2 days, then 500 mg IV/IM q day for 5 days, then 100 mg PO q day until pt no longer at risk<br /> <br /> <br /> If suspect at risk for thiamine deficiency but no sx: thiamine 100 mg PO q day<br /> <br /> <br /> *If you suspect WE/KP/WKS then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high<br /> <br /> *Give magnesium; hypomagnesemic state may be resistant to thiamine administration<br /> <br /> *Give multivitamin; pt at risk for other vitamin deficiencies <br /> <br /> *For chronic alcoholics always consider banana bag: thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W<br /> <br /> ==See Also==<br /> *[[Wernicke's Encephalopathy]]<br /> *[[Wernicke-Korsakoff Syndrome]]<br /> *[[Beriberi]]<br /> *[[Thiamine deficiency]]</div>

Mhankerson https://wikem.org/w/index.php?title=Wernicke-Korsakoff_syndrome&diff=12951 2013-09-19T15:25:33Z

<p>Mhankerson: minor edit</p> <hr /> <div>==Background==<br /> *Wernicke’s Encephalopathy (WE): ACUTE neuro/cardiovascular sx caused by thiamine deficiency<br /> *Korsakoff’s Psychosis (KP): CHRONIC neuro sx caused by thiamine deficiency<br /> *Wernicke-Korsakoff Syndrome (WKS): presence of WE + KP simultaneously <br /> <br /> ==Epidemiology==<br /> *Only 20% identified before death, failure of dx leads to 20% mortality and 75% permanent damage<br /> <br /> ==Causes==<br /> *Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement<br /> **Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis<br /> <br /> ==Pathophysiology==<br /> *Brain lesions/atrophy occurs: mamillary bodies (nearly all cases), thalamus, periaqueductal gray matter, 3rd/4th ventricle, cerebellum, frontal lobe<br /> <br /> ==Diagnosis==<br /> WE/KP/WKS = clinical diagnoses<br /> <br /> <br /> Wernicke’s Encephalopathy<br /> *Classic triad: encephalopathy, oculomotor dysfunction, gait ataxia<br /> *werNICke mnemonic: <br /> **N: Nystagmus/ophthalmoplegia<br /> **I: Incoordination/ataxia<br /> **C: Confusion/memory impairment<br /> *Other sx: hypotension, tachycardia, EKG abnormalities, DOE, CHF sx, hypothermia, coma, dry/wet Beriberi<br /> <br /> <br /> Korsakoff’s Psychosis<br /> *Sx: anterograde/retrograde amnesia, confabulation, confusion, apathy<br /> <br /> <br /> Wernicke-Korsakoff Syndrome<br /> *Sx: combination of WE and KP<br /> <br /> ==Treatment==<br /> If suspect WE/KP/WKS: thiamine 500 mg IV over 30 min TID x 2 days, then 500 mg IV/IM q day for 5 days, then 100 mg PO q day until pt no longer at risk<br /> <br /> <br /> If suspect at risk for thiamine deficiency but no sx: thiamine 100 mg PO q day<br /> <br /> <br /> *If you suspect WE/KP/WKS then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high<br /> <br /> *Give magnesium; hypomagnesemic state may be resistant to thiamine administration<br /> <br /> *Give multivitamin; pt at risk for other vitamin deficiencies <br /> <br /> *For chronic alcoholics always consider banana bag: thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W<br /> <br /> ==See Also==<br /> *[[Wernicke's Encephalopathy]]<br /> *[[Korsakoff's Psychosis]]<br /> *[[Beriberi]]<br /> *[[Thiamine deficiency]]</div>

Mhankerson https://wikem.org/w/index.php?title=Wernicke-Korsakoff_syndrome&diff=12950 2013-09-19T15:23:49Z

<p>Mhankerson: new note</p> <hr /> <div>==Background==<br /> *Wernicke’s Encephalopathy (WE): ACUTE neuro/cardiovascular sx caused by thiamine deficiency<br /> *Korsakoff’s Psychosis (KP): CHRONIC neuro sx caused by thiamine deficiency<br /> *Wernicke-Korsakoff Syndrome (WKS): presence of WE + KP simultaneously <br /> <br /> ==Epidemiology==<br /> *Only 20% identified before death, failure of dx leads to 20% mortality and 75% permanent damage<br /> <br /> ==Causes==<br /> *Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement<br /> **Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis<br /> <br /> ==Pathophysiology==<br /> *Brain lesions/atrophy occurs: mamillary bodies (nearly all cases), thalamus, periaqueductal gray matter, 3rd/4th ventricle, cerebellum, frontal lobe<br /> <br /> ==Diagnosis==<br /> WE/KP/WKS = clinical diagnoses<br /> <br /> <br /> Wernicke’s Encephalopathy<br /> *Classic triad: encephalopathy, oculomotor dysfunction, gait ataxia<br /> *werNICke mnemonic: <br /> **N: Nystagmus/ophthalmoplegia<br /> **I: Incoordination/ataxia<br /> **C: Confusion/memory impairment<br /> *Other sx: hypotension, tachycardia, EKG abnormalities, DOE, CHF sx, hypothermia, coma, dry/wet Beriberi<br /> <br /> <br /> Korsakoff’s Psychosis<br /> *Sx: anterograde/retrograde amnesia, confabulation, confusion, apathy<br /> <br /> <br /> Wernicke-Korsakoff Syndrome<br /> *Sx: combination of WE and KP<br /> <br /> ==Treatment==<br /> If suspect WE/KP/WKS: thiamine 500 mg IV over 30 min TID x 2 days, then 500 mg IV/IM q day for 5 days, then 100 mg PO q day until pt no longer at risk<br /> <br /> <br /> If suspect at risk for thiamine deficiency but no sx: thiamine 100 mg PO q day<br /> <br /> <br /> *If you suspect WE/KP/WKS then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high<br /> <br /> *Give magnesium; hypomagnesemic state may be resistant to thiamine administration<br /> <br /> *Give multivitamin; pt at risk for other vitamin deficiencies <br /> <br /> *For chronic alcoholics always consider banana bag: thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W<br /> <br /> ==See Also==<br /> *[[Wernicke's Encephalopathy]]<br /> *[[Korsakoff's Psychosis]]</div>

Mhankerson https://wikem.org/w/index.php?title=Korsakoff%27s_Psychosis&diff=12949 2013-09-19T15:22:25Z

<p>Mhankerson: new note</p> <hr /> <div>==Background==<br /> *Wernicke’s Encephalopathy (WE): ACUTE neuro/cardiovascular sx caused by thiamine deficiency<br /> *Korsakoff’s Psychosis (KP): CHRONIC neuro sx caused by thiamine deficiency<br /> *Wernicke-Korsakoff Syndrome (WKS): presence of WE + KP simultaneously <br /> <br /> ==Epidemiology==<br /> *Only 20% identified before death, failure of dx leads to 20% mortality and 75% permanent damage<br /> <br /> ==Causes==<br /> *Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement<br /> **Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis<br /> <br /> ==Pathophysiology==<br /> *Brain lesions/atrophy occurs: mamillary bodies (nearly all cases), thalamus, periaqueductal gray matter, 3rd/4th ventricle, cerebellum, frontal lobe<br /> <br /> ==Diagnosis==<br /> WE/KP/WKS = clinical diagnoses<br /> <br /> <br /> Wernicke’s Encephalopathy<br /> *Classic triad: encephalopathy, oculomotor dysfunction, gait ataxia<br /> *werNICke mnemonic: <br /> **N: Nystagmus/ophthalmoplegia<br /> **I: Incoordination/ataxia<br /> **C: Confusion/memory impairment<br /> *Other sx: hypotension, tachycardia, EKG abnormalities, DOE, CHF sx, hypothermia, coma, dry/wet Beriberi<br /> <br /> <br /> Korsakoff’s Psychosis<br /> *Sx: anterograde/retrograde amnesia, confabulation, confusion, apathy<br /> <br /> <br /> Wernicke-Korsakoff Syndrome<br /> *Sx: combination of WE and KP<br /> <br /> ==Treatment==<br /> If suspect WE/KP/WKS: thiamine 500 mg IV over 30 min TID x 2 days, then 500 mg IV/IM q day for 5 days, then 100 mg PO q day until pt no longer at risk<br /> <br /> <br /> If suspect at risk for thiamine deficiency but no sx: thiamine 100 mg PO q day<br /> <br /> <br /> *If you suspect WE/KP/WKS then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high<br /> <br /> *Give magnesium; hypomagnesemic state may be resistant to thiamine administration<br /> <br /> *Give multivitamin; pt at risk for other vitamin deficiencies <br /> <br /> *For chronic alcoholics always consider banana bag: thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W<br /> <br /> ==See Also==<br /> *[[Wernicke's Encephalopathy]]<br /> *[[Wernicke-Korsakoff Syndrome]]</div>

Mhankerson https://wikem.org/w/index.php?title=Wernicke%27s_Encephalopathy&diff=12948 2013-09-19T15:20:43Z

<p>Mhankerson: new note</p> <hr /> <div>==Background==<br /> *Wernicke’s Encephalopathy (WE): ACUTE neuro/cardiovascular sx caused by thiamine deficiency<br /> *Korsakoff’s Psychosis (KP): CHRONIC neuro sx caused by thiamine deficiency<br /> *Wernicke-Korsakoff Syndrome (WKS): presence of WE + KP simultaneously <br /> <br /> ==Epidemiology==<br /> *Only 20% identified before death, failure of dx leads to 20% mortality and 75% permanent damage<br /> <br /> ==Causes==<br /> *Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement<br /> **Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis<br /> <br /> ==Pathophysiology==<br /> *Brain lesions/atrophy occurs: mamillary bodies (nearly all cases), thalamus, periaqueductal gray matter, 3rd/4th ventricle, cerebellum, frontal lobe<br /> <br /> ==Diagnosis==<br /> WE/KP/WKS = clinical diagnoses<br /> <br /> <br /> Wernicke’s Encephalopathy<br /> *Classic triad: encephalopathy, oculomotor dysfunction, gait ataxia<br /> *werNICke mnemonic: <br /> **N: Nystagmus/ophthalmoplegia<br /> **I: Incoordination/ataxia<br /> **C: Confusion/memory impairment<br /> *Other sx: hypotension, tachycardia, EKG abnormalities, DOE, CHF sx, hypothermia, coma, dry/wet Beriberi<br /> <br /> <br /> Korsakoff’s Psychosis<br /> *Sx: anterograde/retrograde amnesia, confabulation, confusion, apathy<br /> <br /> <br /> Wernicke-Korsakoff Syndrome<br /> *Sx: combination of WE and KP<br /> <br /> ==Treatment==<br /> If suspect WE/KP/WKS: thiamine 500 mg IV over 30 min TID x 2 days, then 500 mg IV/IM q day for 5 days, then 100 mg PO q day until pt no longer at risk<br /> <br /> <br /> If suspect at risk for thiamine deficiency but no sx: thiamine 100 mg PO q day<br /> <br /> <br /> *If you suspect WE/KP/WKS then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high<br /> <br /> *Give magnesium; hypomagnesemic state may be resistant to thiamine administration<br /> <br /> *Give multivitamin; pt at risk for other vitamin deficiencies <br /> <br /> *For chronic alcoholics always consider banana bag: thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W<br /> <br /> ==See Also==<br /> *[[Korsakoff's Psychosis]]<br /> *[[Wernicke-Korsakoff Syndrome]]</div>

Mhankerson