WikEM - User contributions [en]

Pulmonary hypertension

2013-09-11T02:15:15Z

Ghasek:

==Background==
Pulmonary Hypertension = mean PA pressure >25mmHg assessed by right heart cath
*can be divided into:
**precapillary PH (normal PCWP)
***Includes Pulmonary arterial hypertension (PAH), PH due to due to lung disease, and chronic thromboembolic PH
**postcapillary PH (elevated PCWP)
***PH due to left heart disease

==Etiology==
*PAH can be heritable, idiopathic, or associated with connective tissue disease, HIV, portal HTN, congenital heart dz, schistosomiasis, chronic hemolytic anemia
*PH can be due to lung disease, left heart disease, chronic exposure to high altitudes, chronic thromboembolic disease, myeloproliferative disorders, sarcoidosis, vasculitis, glycogen storage disease, Gaucher disease, chronic renal failure on dialysis

==Diagnosis==
*Consider in undifferentiated patients with dyspnea, fatigue, syncope, chest pain, palpitations
*Look for JVD, hepatomegaly, ascites, edema, stigmata of liver failure or CTD
*ECG shows signs of RHD (RAE, RAD, RVH)
*CXR with vascular congestion, PA dilation, RA enlargement
*TTE shows fluid status of patient, LV or RV failure, with or without elevated PAP, or pericardial tamponade
*Need RH cath to definitively diagnose

==Chronic Therapies==
*Prostacyclins - vasodilatation, inhibit platelet aggregation
**Epoprostenol, Iloprost, Treprostinil, Beraprost
**Complications include acute decompensation if stopped abruptly, diarrhea, edema, headache
*Phosphodiesterase Type 5 (PDE5) Inhibitors - vasodilation, increases RV contractility
**Sildenafil
**Complications include hypotension with administration of nitrates, flushing, epistaxis, headache
*Endothelin receptor antagonists - vasodilation
**Bosentan, Ambrisentan
** Complications include liver failure, supratherapeutic INR,
*Patients also usually taking digoxin, coumadin, diuretics, home O2. RARELY are they on CCB only if responsive during cath. Consider line infections as complication to chronic infusions.

==Acute Treatment for PAH crisis==
# Decrease preload - no fluids, consider diuretics
# O2
# Optimize myocardial contractility
##Treat relative bradycardia
###atropine, pace, low dose dobutamine <5mcg/kg/min to increase contractility
###Consider norepinephrine prior to dobutamine if hypotensive
##Rhythm control for tachycardias - NO CCB or BB for rate control
###Electrical cardioversion or amiodarone
# Decrease afterload - pulmonary vasodilation
##sildenafil, bostantan, epoprostenol (2ng/kg/min), inhaled NO if intubated
# Check INR, dig level and correct
# Empiric abx
# If intubated, low PEEP, low tidal volumes

==Source==
*4/07 DONALDSON (adapted from Sarver)
*Critical Decisions in Emergency Medicine, May 2013; 27(5)

[[Category:Cards]]
[[Category:Pulm]]

Pulmonary hypertension

2013-09-11T02:03:14Z

Ghasek:

==Background==
Pulmonary Hypertension = mean PA pressure >25mmHg assessed by right heart cath
*can be divided into:
**precapillary PH (normal PCWP)
***Includes Pulmonary arterial hypertension (PAH), PH due to due to lung disease, and chronic thromboembolic PH
**postcapillary PH (elevated PCWP)
***PH due to left heart disease

==Etiology==
*PAH can be heritable, idiopathic, or associated with connective tissue disease, HIV, portal HTN, congenital heart dz, schistosomiasis, chronic hemolytic anemia
*PH can be due to lung disease, left heart disease, chronic exposure to high altitudes, chronic thromboembolic disease, myeloproliferative disorders, sarcoidosis, vasculitis, glycogen storage disease, Gaucher disease, chronic renal failure on dialysis

==Diagnosis==
*Consider in undifferentiated patients with dyspnea, fatigue, syncope, chest pain, palpitations
*Look for JVD, hepatomegaly, ascites, edema, stigmata of liver failure or CTD
*ECG shows signs of RHD (RAE, RAD, RVH)
*CXR with vascular congestion, PA dilation, RA enlargement
*TTE shows elevated PAP
*Need RH cath to diagnose

==Chronic Therapies==
*Prostacyclins - vasodilatation, inhibit platelet aggregation
**Epoprostenol, Iloprost, Treprostinil, Beraprost
**Complications include acute decompensation if stopped abruptly, diarrhea, edema, headache
*Phosphodiesterase Type 5 (PDE5) Inhibitors - vasodilation, increases RV contractility
**Sildenafil
**Complications include hypotension with administration of nitrates, flushing, epistaxis, headache
*Endothelin receptor antagonists - vasodilation
**Bosentan, Ambrisentan
** Complications include liver failure, supratherapeutic INR,
*Patients also usually taking digoxin, coumadin, diuretics, home O2. RARELY are they on CCB only if responsive during cath. Consider line infections as complication to chronic infusions.

==Acute Treatment for PAH crisis==
# No fluids, consider diuretics
# O2
# Treat relative bradycardia
##atropine, pace, low dose dobutamine <5mcg/kg/min to increase contractility
##Consider norepinephrine prior to dobutamine if hypotensive
#Cardiovert tachycardias - NO CCB or BB
##Electrical cardioversion or amiodarone
# Pulm vasodialate
##sildenafil, bostantan, epoprostenol (2ng/kg/min), inhaled NO if intubated
# Check INR, dig level and correct
# Empiric abx
# If intubated, low PEEP, low tidal volumes

==Source==
4/07 DONALDSON (adapted from Sarver)

[[Category:Cards]]
[[Category:Pulm]]

Pulmonary hypertension

2013-09-11T01:54:34Z

Ghasek:

==Background==
Pulmonary Hypertension = mean PA pressure >25mmHg assessed by right heart cath
*can be divided into:
**precapillary PH (normal PCWP)
***Includes Pulmonary arterial hypertension (PAH), PH due to due to lung disease, and chronic thromboembolic PH
**postcapillary PH (elevated PCWP)
***PH due to left heart disease

==Etiology==
*PAH can be heritable, idiopathic, or associated with connective tissue disease, HIV, portal HTN, congenital heart dz, schistosomiasis, chronic hemolytic anemia
*PH can be due to lung disease, left heart disease, chronic exposure to high altitudes, chronic thromboembolic disease, myeloproliferative disorders, sarcoidosis, vasculitis, glycogen storage disease, Gaucher disease, chronic renal failure on dialysis

==Diagnosis==
*Consider in undifferentiated patients with dyspnea, fatigue, syncope, chest pain, palpitations
*Look for JVD, hepatomegaly, ascites, edema, stigmata of liver failure or CTD
*ECG shows signs of RHD (RAE, RAD, RVH)
*CXR with vascular congestion, PA dilation, RA enlargement
*TTE shows elevated PAP
*Need RH cath to diagnose

==Chronic Therapies==
*Prostacyclins - vasodilatation, inhibit platelet aggregation
**Epoprostenol, Iloprost, Treprostinil, Beraprost
**Complications include acute decompensation if stopped abruptly, diarrhea, edema, headache
*Phosphodiesterase Type 5 (PDE5) Inhibitors - vasodilation, increases RV contractility
**Sildenafil
**Complications include hypotension with administration of nitrates, flushing, epistaxis, headache
*Endothelin receptor antagonists - vasodilation
**Bosentan, Ambrisentan
** Complications include liver failure, supratherapeutic INR,
*Patients also usually taking digoxin, coumadin, diuretics, home O2. RARELY are they on CCB only if responsive during cath

==Acute Treatment for PAH crisis==
# No fluids
# O2
# Treat relative bradycardia
##atropine, pace, dobutamine
#Cardiovert tachycardias - NO CCB or BB
##Electrical cardioversion or amiodarone
# Pulm vasodialate
##sildenafil, bostantan
# check INR, dig level and correct
# Empiric abx

==Source==
4/07 DONALDSON (adapted from Sarver)

[[Category:Cards]]
[[Category:Pulm]]

Pulmonary hypertension

2013-09-11T01:11:40Z

Ghasek:

Sepsis (peds)

2013-09-11T01:00:27Z

Ghasek:

==Background==
*Neonatal Sepsis
**Early onset
***First few days of life
***Fulminant, assoc w/ maternal or perinatal risk factors
***Septic shock and neutropenia are more common
**Late onset
***Occurs after 1wk of age
***Gradual
***Meningitis more likely
**Consider if feeding disturbance, rash, lethargy, irritability, sz, apnea, tachypnea, grunting, vomiting, poor PO, gastric distention, diarrhea

==Diagnosis==
*SIRS criteria in peds needs > or equal to 2 of 4 requirements, with abnormal temp or WBC required
**Temperature >100.4 or <96.8
**Age specific tachycardia or bradycardia <10th % for age <1 year
** RR >2 SD above the norm
** WBC elevated or depressed, based on age, or >10% bands

*SEVERE SEPSIS includes
**Cardiovascular organ dysfunction
**Respiratory distress
*OR
**CNS dysfunction - GCS <11 or >3 loss from baseline
**Platelets <80 or >50% decrease from baseline
**Creatinine >2x upper limit of normal/baseline
**Total bilirubin >4 or ALT >2x normal

*SEPTIC SHOCK includes
**hypotension <5th % for age, or SBP <2 SD below normal for age
*OR
**needs for vasoactive drugs to maintain BP
*OR
**metabolic acidosis base deficit >5
**arterial lactate >2x normal
**UOP <0.5 mL/kg/hr
**capillary refill >5 sec
**core to peripheral temp gap >3 degrees C
*DESPITE IVF resuscitation >40mL/kg in 1 hour

==Work-Up==
#CBC, CMP, arterial lactate
#UA/Ucx
#CXR
#CSF
#Blood Cx

==Treatment==
*Neonatal
**Ampicillin 50mg/kg + gentamicin 2.5mg/kg + acyclovir
***If gram-negative strongly suspected replace gent w/ cefotaxime or ceftaz
****Have better CNS penetration

*GOLDEN HOUR goals of resuscitation:
**Cap refill <2 sec
**Normal BP
**Normal pulses, similar central and peripheral
**Warm extremities
**UOP >1 mL/kg/hr
**Normal mental status

*If vasopressors needed for septic shock, follow recommendations:
**Normotensive shock with impaired perfusion: dopamine
**Warm shock (vasodilated with poor perfusion or low BP): norepinephrine
**Cold shock (vasoconstricted with poor perfusion or low BP): epinephrine

*Consider steroids if fluid-refractory, catecholamine-resistant shock or suspected or known adrenal insufficiency
**Consider AI in septic shock with purpura, chronic steroid use, hx of pituitary or adrenal abnormalities

*Transfuse if Scvo2 <70 and Hgb <10
*Transfuse platelets if <10 without bleeding, or <20 with high risk of bleed

==Disposition==
*Admit all neonates

==See Also==
[[Pediatric Fever]]

==Source==
Tintinalli
"Pediatric Sepsis" published in EM Resident 2013 40(4) , adapted from Goldstein, et al. Pediatr Crit Care Med 2005; 6:2-8.

[[Category:Peds]]

Epinephrine

2013-04-17T19:36:49Z

Ghasek: /* Anaphylaxis */

==Concentration==
#Amount of solution in mL used to dilute 1,000mg of epinephrine
##eg 1:10,000 = 1,000mg/10,000mL = 0.1mg/mL

==[[Anaphylaxis]]==
0.3-0.5mg of 1:1,000 IM
*Consider glucagon 1-5mg IV if pt on B-blockers and not responding to epi

==Anaphylactic Shock==
0.1mg of 1:10,000 slow IV during 5 min, can start infusion of 1-4 mcg/min

==Cardiac Arrest==
1mg of 1:10,000 IVP

==See Also==
[[Digital EpiPen Injection ]]

[[Category:Drugs]]
[[Category:Airway/Resus]]

Epinephrine

2013-04-17T19:35:21Z

Ghasek: /* Anaphylactic Shock */

==Concentration==
#Amount of solution in mL used to dilute 1,000mg of epinephrine
##eg 1:10,000 = 1,000mg/10,000mL = 0.1mg/mL

==[[Anaphylaxis]]==
0.3-0.5mg of 1:1,000 IM

==Anaphylactic Shock==
0.1mg of 1:10,000 slow IV during 5 min, can start infusion of 1-4 mcg/min

==Cardiac Arrest==
1mg of 1:10,000 IVP

==See Also==
[[Digital EpiPen Injection ]]

[[Category:Drugs]]
[[Category:Airway/Resus]]

Angioedema

2013-04-17T19:33:03Z

Ghasek: /* Treatment */

==Background==
*Angioedema is paroxysmal, nondemarcated swelling of dermal or submucosal layers of skin or mucosa
**Swelling is asymmetric, nonpitting, and nonpruritic
*4 etiologies:
**1. Congenital or acquired loss of C1 esterase inhibitor
**2. IgE–mediated type I allergic reaction
**3. ACEI adverse reaction
**4. Idiopathic

==Hereditary Angioedema==
===Background===
*Due to C1 esterase inhibitor deficiency
**Leads to unregulated activity of vasoactive mediators (bradykinin) associated with complement pathway
**Autosomal dominant

===Diagnosis===
*Suspect in patients with history of recurrent peripheral angioedema and abdominal pain
**75% experience onset of symptoms before age 15yr
*C4 level screens for HAE (suspect if low)
*Decreased levels of C1 and C4 esterase inhibitors confirms diagnosis

===Treatment===
*Strongly consider definitive airway if voice change, hoarseness, stridor, dyspnea - arrange transfer to OR if not crashing
*Epinephrine can produce some improvement in early acute attacks associated with anaphylaxis, however, HAE is bradykinin mediated and the role of steroids and H1/H2 blockers is limited
*If available - C1 esterase inhibitors (Berinert 20u/kg IV), kallikrein/bradykinin inhibitors (ecallantide 30mg SQ), or bradykinin receptor antagonist (icantibant 30mg SQ)
*FFP
**Replaces the missing inhibitor protein
**Not recommended in life-threatening laryngeal edema (some pts may become more edematous)
***Instead, pt should undergo fiberoptic intubation w/ preparation for surgical airway

==ACE Inhibitor-induced Angioedema==
===Background===
*Incidence is highest within the first month; however, may occur at anytime
*Incidence is 0.1-2.2% (more common in blacks)
*Physiology more closely related to bradykinin-mediated pathway than IgE-mediated pathway, therefore current treatments may be insufficient

===Treatment===
*Airway management as above, consider awake fiberoptic intubation
*Epinephrine 0.3mg IM q15-20min prn
*Consider glucagon 1-5mg IV if pt on B-blockers and not responding to epi
*Diphenhydramine 50mg IV OR cetirizine 10mg PO
*Methylprednisolone 125mg IV
*H2 blocker IV or PO

==Disposition==
*Consider discharge after 4-6 hrs obs if there is no airway edema and pt improves
*24 hrs obs if epi given
*Ishoo Staging (based on retrospective study)
**Stage 1 - face/lip
***48% outpatient, 52% floor, 0% ICU or advanced airway
**Stage 2 - soft palate
***60% outpt, 40% floor, 0 ICU or advanced airway
**Stage 3 - tongue
***26% outpt, 67% ICU, 7% advanced airway
**Stage 4 - larynx
***100% ICU, 24% advanced airway

==See Also==
*[[Anaphylaxis]]
*[[Tongue pathology]]

==Source==
*Tintinalli
*EB Medicine "Angioedema in the Emergency Department: An Evidence Based Review" Nov 2012
*Ishoo, et al, 1999, "Predicting Airway Risk in Angioedema: staging system based on presentation" in Otolaryngology - Head and Neck Surgery
[[Category:ENT]]

Angioedema

2013-04-17T19:30:37Z

Ghasek: /* Treatment */

==Background==
*Angioedema is paroxysmal, nondemarcated swelling of dermal or submucosal layers of skin or mucosa
**Swelling is asymmetric, nonpitting, and nonpruritic
*4 etiologies:
**1. Congenital or acquired loss of C1 esterase inhibitor
**2. IgE–mediated type I allergic reaction
**3. ACEI adverse reaction
**4. Idiopathic

==Hereditary Angioedema==
===Background===
*Due to C1 esterase inhibitor deficiency
**Leads to unregulated activity of vasoactive mediators (bradykinin) associated with complement pathway
**Autosomal dominant

===Diagnosis===
*Suspect in patients with history of recurrent peripheral angioedema and abdominal pain
**75% experience onset of symptoms before age 15yr
*C4 level screens for HAE (suspect if low)
*Decreased levels of C1 and C4 esterase inhibitors confirms diagnosis

===Treatment===
*Strongly consider definitive airway if voice change, hoarseness, stridor, dyspnea - arrange transfer to OR if not crashing
*Epinephrine can produce some improvement in early acute attacks associated with anaphylaxis, however, HAE is bradykinin mediated and the role of steroids and H1/H2 blockers is limited
*If available - C1 esterase inhibitors (Berinert 20u/kg IV), kallikrein/bradykinin inhibitors (ecallantide 30mg SQ), or bradykinin receptor antagonist (icantibant 30mg SQ)
*FFP
**Replaces the missing inhibitor protein
**Not recommended in life-threatening laryngeal edema (some pts may become more edematous)
***Instead, pt should undergo fiberoptic intubation w/ preparation for surgical airway

==ACE Inhibitor-induced Angioedema==
===Background===
*Incidence is highest within the first month; however, may occur at anytime
*Incidence is 0.1-2.2% (more common in blacks)
*Physiology more closely related to bradykinin-mediated pathway than IgE-mediated pathway, therefore current treatments may be insufficient

===Treatment===
*Epinephrine 0.3mg IM q15-20min prn
*Diphenhydramine 50mg IV OR cetirizine 10mg PO
*Methylprednisolone 125mg IV
*Awake fiberoptic intubation

==Disposition==
*Consider discharge after 4-6 hrs obs if there is no airway edema and pt improves
*24 hrs obs if epi given
*Ishoo Staging (based on retrospective study)
**Stage 1 - face/lip
***48% outpatient, 52% floor, 0% ICU or advanced airway
**Stage 2 - soft palate
***60% outpt, 40% floor, 0 ICU or advanced airway
**Stage 3 - tongue
***26% outpt, 67% ICU, 7% advanced airway
**Stage 4 - larynx
***100% ICU, 24% advanced airway

==See Also==
*[[Anaphylaxis]]
*[[Tongue pathology]]

==Source==
*Tintinalli
*EB Medicine "Angioedema in the Emergency Department: An Evidence Based Review" Nov 2012
*Ishoo, et al, 1999, "Predicting Airway Risk in Angioedema: staging system based on presentation" in Otolaryngology - Head and Neck Surgery
[[Category:ENT]]

Angioedema

2013-04-17T19:20:23Z

Ghasek: /* Source */

==Background==
*Angioedema is paroxysmal, nondemarcated swelling of dermal or submucosal layers of skin or mucosa
**Swelling is asymmetric, nonpitting, and nonpruritic
*4 etiologies:
**1. Congenital or acquired loss of C1 esterase inhibitor
**2. IgE–mediated type I allergic reaction
**3. ACEI adverse reaction
**4. Idiopathic

==Hereditary Angioedema==
===Background===
*Due to C1 esterase inhibitor deficiency
**Leads to unregulated activity of vasoactive mediators (bradykinin) associated with complement pathway
**Autosomal dominant

===Diagnosis===
*Suspect in patients with history of recurrent peripheral angioedema and abdominal pain
**75% experience onset of symptoms before age 15yr
*C4 level screens for HAE (suspect if low)
*Decreased levels of C1 and C4 esterase inhibitors confirms diagnosis

===Treatment===
*Epinephrine can produce some improvement in early acute attacks associated with anaphylaxis, however, HAE is bradykinin mediated and the role of steroids and H1/H2 blockers is limited
*If available - C1 esterase inhibitors (Berinert 20u/kg IV), kallikrein/bradykinin inhibitors (ecallantide 30mg SQ), or bradykinin receptor antagonist (icantibant 30mg SQ)
*FFP
**Replaces the missing inhibitor protein
**Not recommended in life-threatening laryngeal edema (some pts may become more edematous)
***Instead, pt should undergo fiberoptic intubation w/ preparation for surgical airway

==ACE Inhibitor-induced Angioedema==
===Background===
*Incidence is highest within the first month; however, may occur at anytime
*Incidence is 0.1-2.2% (more common in blacks)
*Physiology more closely related to bradykinin-mediated pathway than IgE-mediated pathway, therefore current treatments may be insufficient

===Treatment===
*Epinephrine 0.3mg IM q15-20min prn
*Diphenhydramine 50mg IV OR cetirizine 10mg PO
*Methylprednisolone 125mg IV
*Awake fiberoptic intubation

==Disposition==
*Consider discharge after 4-6 hrs obs if there is no airway edema and pt improves
*24 hrs obs if epi given
*Ishoo Staging (based on retrospective study)
**Stage 1 - face/lip
***48% outpatient, 52% floor, 0% ICU or advanced airway
**Stage 2 - soft palate
***60% outpt, 40% floor, 0 ICU or advanced airway
**Stage 3 - tongue
***26% outpt, 67% ICU, 7% advanced airway
**Stage 4 - larynx
***100% ICU, 24% advanced airway

==See Also==
*[[Anaphylaxis]]
*[[Tongue pathology]]

==Source==
*Tintinalli
*EB Medicine "Angioedema in the Emergency Department: An Evidence Based Review" Nov 2012
*Ishoo, et al, 1999, "Predicting Airway Risk in Angioedema: staging system based on presentation" in Otolaryngology - Head and Neck Surgery
[[Category:ENT]]

Angioedema

2013-04-17T19:18:36Z

Ghasek: /* Source */

==Background==
*Angioedema is paroxysmal, nondemarcated swelling of dermal or submucosal layers of skin or mucosa
**Swelling is asymmetric, nonpitting, and nonpruritic
*4 etiologies:
**1. Congenital or acquired loss of C1 esterase inhibitor
**2. IgE–mediated type I allergic reaction
**3. ACEI adverse reaction
**4. Idiopathic

==Hereditary Angioedema==
===Background===
*Due to C1 esterase inhibitor deficiency
**Leads to unregulated activity of vasoactive mediators (bradykinin) associated with complement pathway
**Autosomal dominant

===Diagnosis===
*Suspect in patients with history of recurrent peripheral angioedema and abdominal pain
**75% experience onset of symptoms before age 15yr
*C4 level screens for HAE (suspect if low)
*Decreased levels of C1 and C4 esterase inhibitors confirms diagnosis

===Treatment===
*Epinephrine can produce some improvement in early acute attacks associated with anaphylaxis, however, HAE is bradykinin mediated and the role of steroids and H1/H2 blockers is limited
*If available - C1 esterase inhibitors (Berinert 20u/kg IV), kallikrein/bradykinin inhibitors (ecallantide 30mg SQ), or bradykinin receptor antagonist (icantibant 30mg SQ)
*FFP
**Replaces the missing inhibitor protein
**Not recommended in life-threatening laryngeal edema (some pts may become more edematous)
***Instead, pt should undergo fiberoptic intubation w/ preparation for surgical airway

==ACE Inhibitor-induced Angioedema==
===Background===
*Incidence is highest within the first month; however, may occur at anytime
*Incidence is 0.1-2.2% (more common in blacks)
*Physiology more closely related to bradykinin-mediated pathway than IgE-mediated pathway, therefore current treatments may be insufficient

===Treatment===
*Epinephrine 0.3mg IM q15-20min prn
*Diphenhydramine 50mg IV OR cetirizine 10mg PO
*Methylprednisolone 125mg IV
*Awake fiberoptic intubation

==Disposition==
*Consider discharge after 4-6 hrs obs if there is no airway edema and pt improves
*24 hrs obs if epi given
*Ishoo Staging (based on retrospective study)
**Stage 1 - face/lip
***48% outpatient, 52% floor, 0% ICU or advanced airway
**Stage 2 - soft palate
***60% outpt, 40% floor, 0 ICU or advanced airway
**Stage 3 - tongue
***26% outpt, 67% ICU, 7% advanced airway
**Stage 4 - larynx
***100% ICU, 24% advanced airway

==See Also==
*[[Anaphylaxis]]
*[[Tongue pathology]]

==Source==
Tintinalli
EB Medicine "Angioedema in the Emergency Department: An Evidence Based Review" Nov 2012
Ishoo, et al, 1999, "Predicting Airway Risk in Angioedema: staging system based on presentation" in Otolaryngology - Head and Neck Surgery
[[Category:ENT]]

Angioedema

2013-04-17T19:15:22Z

Ghasek: /* Disposition */

==Background==
*Angioedema is paroxysmal, nondemarcated swelling of dermal or submucosal layers of skin or mucosa
**Swelling is asymmetric, nonpitting, and nonpruritic
*4 etiologies:
**1. Congenital or acquired loss of C1 esterase inhibitor
**2. IgE–mediated type I allergic reaction
**3. ACEI adverse reaction
**4. Idiopathic

==Hereditary Angioedema==
===Background===
*Due to C1 esterase inhibitor deficiency
**Leads to unregulated activity of vasoactive mediators (bradykinin) associated with complement pathway
**Autosomal dominant

===Diagnosis===
*Suspect in patients with history of recurrent peripheral angioedema and abdominal pain
**75% experience onset of symptoms before age 15yr
*C4 level screens for HAE (suspect if low)
*Decreased levels of C1 and C4 esterase inhibitors confirms diagnosis

===Treatment===
*Epinephrine can produce some improvement in early acute attacks associated with anaphylaxis, however, HAE is bradykinin mediated and the role of steroids and H1/H2 blockers is limited
*If available - C1 esterase inhibitors (Berinert 20u/kg IV), kallikrein/bradykinin inhibitors (ecallantide 30mg SQ), or bradykinin receptor antagonist (icantibant 30mg SQ)
*FFP
**Replaces the missing inhibitor protein
**Not recommended in life-threatening laryngeal edema (some pts may become more edematous)
***Instead, pt should undergo fiberoptic intubation w/ preparation for surgical airway

==ACE Inhibitor-induced Angioedema==
===Background===
*Incidence is highest within the first month; however, may occur at anytime
*Incidence is 0.1-2.2% (more common in blacks)
*Physiology more closely related to bradykinin-mediated pathway than IgE-mediated pathway, therefore current treatments may be insufficient

===Treatment===
*Epinephrine 0.3mg IM q15-20min prn
*Diphenhydramine 50mg IV OR cetirizine 10mg PO
*Methylprednisolone 125mg IV
*Awake fiberoptic intubation

==Disposition==
*Consider discharge after 4-6 hrs obs if there is no airway edema and pt improves
*24 hrs obs if epi given
*Ishoo Staging (based on retrospective study)
**Stage 1 - face/lip
***48% outpatient, 52% floor, 0% ICU or advanced airway
**Stage 2 - soft palate
***60% outpt, 40% floor, 0 ICU or advanced airway
**Stage 3 - tongue
***26% outpt, 67% ICU, 7% advanced airway
**Stage 4 - larynx
***100% ICU, 24% advanced airway

==See Also==
*[[Anaphylaxis]]
*[[Tongue pathology]]

==Source==
Tintinalli

[[Category:ENT]]

Angioedema

2013-04-17T19:06:18Z

Ghasek: /* ACE Inhibitor-induced Angioedema */

==Background==
*Angioedema is paroxysmal, nondemarcated swelling of dermal or submucosal layers of skin or mucosa
**Swelling is asymmetric, nonpitting, and nonpruritic
*4 etiologies:
**1. Congenital or acquired loss of C1 esterase inhibitor
**2. IgE–mediated type I allergic reaction
**3. ACEI adverse reaction
**4. Idiopathic

==Hereditary Angioedema==
===Background===
*Due to C1 esterase inhibitor deficiency
**Leads to unregulated activity of vasoactive mediators (bradykinin) associated with complement pathway
**Autosomal dominant

===Diagnosis===
*Suspect in patients with history of recurrent peripheral angioedema and abdominal pain
**75% experience onset of symptoms before age 15yr
*C4 level screens for HAE (suspect if low)
*Decreased levels of C1 and C4 esterase inhibitors confirms diagnosis

===Treatment===
*Epinephrine can produce some improvement in early acute attacks associated with anaphylaxis, however, HAE is bradykinin mediated and the role of steroids and H1/H2 blockers is limited
*If available - C1 esterase inhibitors (Berinert 20u/kg IV), kallikrein/bradykinin inhibitors (ecallantide 30mg SQ), or bradykinin receptor antagonist (icantibant 30mg SQ)
*FFP
**Replaces the missing inhibitor protein
**Not recommended in life-threatening laryngeal edema (some pts may become more edematous)
***Instead, pt should undergo fiberoptic intubation w/ preparation for surgical airway

==ACE Inhibitor-induced Angioedema==
===Background===
*Incidence is highest within the first month; however, may occur at anytime
*Incidence is 0.1-2.2% (more common in blacks)
*Physiology more closely related to bradykinin-mediated pathway than IgE-mediated pathway, therefore current treatments may be insufficient

===Treatment===
*Epinephrine 0.3mg IM q15-20min prn
*Diphenhydramine 50mg IV OR cetirizine 10mg PO
*Methylprednisolone 125mg IV
*Awake fiberoptic intubation

==Disposition==
*Consider discharge after obs if there is no airway edema and pt improves

==See Also==
*[[Anaphylaxis]]
*[[Tongue pathology]]

==Source==
Tintinalli

[[Category:ENT]]

Angioedema

2013-04-17T18:56:11Z

Ghasek: /* Treatment */

Angioedema

2013-04-17T18:48:14Z

Ghasek: /* Background */

Angioedema

2013-04-17T18:45:58Z

Ghasek: /* Diagnosis */

Adrenal crisis

2012-08-15T18:31:27Z

Ghasek:

==Background==
*Consider in any pt w/ unexplained hypotension (esp if have HIV or take steroids)
*Main factor causing adrenal crisis is mineralocorticoid, not glucocorticoid, deficiency
**This is the reason crises occur much more frequently w/ primary adrenal insufficiency
*Major clinical problem is hypotension
**Most commonly presents as shock

==Causes (Adrenal Insufficiency)==
#Primary adrenal insufficiency (decreased cortisol and aldosterone)
##Autoimmune (70%)
##Adrenal hemorrhage
###Coagulation disorders
###Sepsis (Waterhouse-Friderichsen syndrome)
##Meds
##Infection (HIV, TB)
##Sarcoidosis/amyloidosis
##Mets
##[[Congenital Adrenal Hyperplasia|CAH]]
#Secondary adrenal insufficiency (decreased ACTH -> decreased cortisol only)
##Withdrawal of steroid therapy
##Pituitary disease
##Head trauma
##Postpartum pituitary necrosis
##Infiltrative disorders of pituitary or hypothalamus

==Precipitants==
*Increased demand
**Infection
**MI
**Surgery
**Trauma
*Decreased supply
**Discontinuation of steriod therapy

==Clinical Features==
*Hypotension
**Refractory to fluids/presors
*Dehydration
*Abdominal tenderness
**Usually generalized
*Hyponatremia/hyperkalemia
*Hypoglycemia
*Confusion/delirium/lethargy
*Fever
**Usually caused by infection

==Workup==
#Chemistry
#Random cortisol, renin, and ACTH levels
##Do not wait for levels before starting treatment

==Treatment==
#Begin tx immediately in any suspected case(prognosis related to rapidity of tx)
#IVF
##D5NS IV 2-3L (corrects fluid deficit and hypoglycemia)
#Steroids
##Hydrocortisone
###Drug of choice if K+>6 (provides glucocorticoid and mineralcorticoid effects)
###2mg/kg up to 100mg IV bolus
##Dexamethasone
###Consider in stable patients if ACTH stim test will be performed (won't interfere w/ the test)
###4mg IV bolus
#Vasopressors
##Administered after steriod therapy in pts unresponsive to fluid resuscitation
#Treat underlying cause

==See Also==
*[[Congenital Adrenal Hyperplasia]]

==Source ==
Tintinalli's
ACEP Critical Decisions in Emergency Medicine July 2012 issue

[[Category:Endo]]

Vasopressors

2011-10-15T22:51:13Z

Ghasek: /* Indication */

==Norepinephrine==
===Indication===
*Septic shock

===Dosing===
*Start 2mcg/min
**Incr by 1-2mcg/min q3-5min prn
**Max dose is 30mcg/min
*Replace volume before starting

===Adverse Effects===
*If extravasates use phentolamine 5-10mg into affected area

===Mechanism of Action===
*Alpha and beta1 agonist
**Incr contractility, HR
**Arterial/venous vasoconstriction

==Dopamine==
===Indication===
*Hypotension caused by:
**Septic shock
**MI
**Trauma/spinal shock
**Heart failure

===Contraindication===
*Tachyarrhythmias

===Dosing===
*Use lowest dose possible (prevent tachyphylaxis)
**3-20mcg/kg/min works for most
*May use in peripheral IV temporarily
**Avoid using in same line as alkaline infusions

===Adverse Effects===
*Low doses
**Hypotension
*High doses
**Hypertension, ectopic beats
*Tissue necrosis (if extravasates)
**If occurs use phentolamine 5-10mg in affected area

===Mechanism of Action===
*0-5mcg/kg/min
**Vasodilation (renal, mesenteric, coronary)
*5-10mcg/kg/min
**Beta1, alpha1 agonist
***Incr CO, contractility, vasoconstriction
*>10mcg/kg/min
**Alpha effects predominate

==Dobutamine==
===Indication===
*Cardiogenic shock
*Low-output heart failure
*Tricyclic overdose

===Dosing===
*2-20mcg/kg/min
**10mcg works for most
*May use in peripheral IV
===Adverse Effects===
*Modest incr in HR/BP
*PVCs
*B2 effect may result in vasodilation
**Caution if sys BP <90

===Mechanism of Action===
*Primarily B1 (and B2) agonist
**Increases CO via incr contractility

==Phenylephrine==
===Indication===
*Shock

===Dosing===
*Start 100-200mcg/min then taper down
**40-60mcg/min works for most

===Adverse Effects===
*Bradycardia
*If extravasates use phentolamine

===Mechanism of Action===
*Alpha agonist
**Vasoconstriction w/ reflex decr HR
***May decrease stroke volume

==Push Dose Pressors==
*Use when need temporary BP or CO boost
**Post-intubation hypotension
**Propofol-induced hypotension
**A-fib w/ hypotension
***Easier to convert well-perfused heart

===Epinephrine===
*Mix 9mL of NS with 1mL of 1:10,000 epi
**Now have 10mL of 10mcg/mL
***Use 0.5-2mL q2-5min (similar to epi drip)
***Same as 2% lido with epi
****Ok to give peripherally
*Onset - 1min
*Duration - 5-10min

===Phenylephrine===
*Pure alpha (no effect on heart)
*Place 1mL of 10mg/mL in 100mL NS
**Draw up 10mL
***Now have 100mcg/mL
**Use 0.5-2mL q2-5min
*Onset - 1min
*Duration - 20min

== Source ==
Tintinalli

EmCrit Podcast 6
[[Category:Drugs]]
[[Category:Airway/Resus]]

Vasopressors

2011-10-15T22:50:27Z

Ghasek: /* Indication */

==Norepinephrine==
===Indication===
*Septic shock

===Dosing===
*Start 2mcg/min
**Incr by 1-2mcg/min q3-5min prn
**Max dose is 30mcg/min
*Replace volume before starting

===Adverse Effects===
*If extravasates use phentolamine 5-10mg into affected area

===Mechanism of Action===
*Alpha and beta1 agonist
**Incr contractility, HR
**Arterial/venous vasoconstriction

==Dopamine==
===Indication===
*Hypotension caused by:
**Septic shock
**MI
**Trauma
**Heart failure

===Contraindication===
*Tachyarrhythmias

===Dosing===
*Use lowest dose possible (prevent tachyphylaxis)
**3-20mcg/kg/min works for most
*May use in peripheral IV temporarily
**Avoid using in same line as alkaline infusions

===Adverse Effects===
*Low doses
**Hypotension
*High doses
**Hypertension, ectopic beats
*Tissue necrosis (if extravasates)
**If occurs use phentolamine 5-10mg in affected area

===Mechanism of Action===
*0-5mcg/kg/min
**Vasodilation (renal, mesenteric, coronary)
*5-10mcg/kg/min
**Beta1, alpha1 agonist
***Incr CO, contractility, vasoconstriction
*>10mcg/kg/min
**Alpha effects predominate

==Dobutamine==
===Indication===
*Cardiogenic shock
*Low-output heart failure
*Tricyclic overdose

===Dosing===
*2-20mcg/kg/min
**10mcg works for most
*May use in peripheral IV
===Adverse Effects===
*Modest incr in HR/BP
*PVCs
*B2 effect may result in vasodilation
**Caution if sys BP <90

===Mechanism of Action===
*Primarily B1 (and B2) agonist
**Increases CO via incr contractility

==Phenylephrine==
===Indication===
*Shock

===Dosing===
*Start 100-200mcg/min then taper down
**40-60mcg/min works for most

===Adverse Effects===
*Bradycardia
*If extravasates use phentolamine

===Mechanism of Action===
*Alpha agonist
**Vasoconstriction w/ reflex decr HR
***May decrease stroke volume

==Push Dose Pressors==
*Use when need temporary BP or CO boost
**Post-intubation hypotension
**Propofol-induced hypotension
**A-fib w/ hypotension
***Easier to convert well-perfused heart

===Epinephrine===
*Mix 9mL of NS with 1mL of 1:10,000 epi
**Now have 10mL of 10mcg/mL
***Use 0.5-2mL q2-5min (similar to epi drip)
***Same as 2% lido with epi
****Ok to give peripherally
*Onset - 1min
*Duration - 5-10min

===Phenylephrine===
*Pure alpha (no effect on heart)
*Place 1mL of 10mg/mL in 100mL NS
**Draw up 10mL
***Now have 100mcg/mL
**Use 0.5-2mL q2-5min
*Onset - 1min
*Duration - 20min

== Source ==
Tintinalli

EmCrit Podcast 6
[[Category:Drugs]]
[[Category:Airway/Resus]]

Metabolic alkalosis

2011-08-02T20:40:18Z

Ghasek:

==Background==
*pH > 7.42 = alkalemia
*HCO3 > 28 = metabolic alkalosis
*Always determine if there is also a concurrent primary respiratory process
**expected pCO2 = 40 + 0.6(measured HCO3 - 24)
**if pCO2>pCO2 expected, then there is also a primary respiratory acidosis
**if pCO2<pCO2 expected, then there is also primary respiratory alkalosis
*Always calculate AG to determine if concurrent primary metabolic acidosis

==Pathophysiology==
*Chloride-Responsive (volume depletion)
**Condition that produces chloride loss also tends to reduce extracellular volume
***Reduction in extracellular volume increases mineralocorticoid activity
****Enhances Na reabsorption and K+/H+ secretion in renal tubule
*****K/H+ secretion -> HCO3 generation
******Resulting urine is alkaline with little chloride (<10)
*Chloride-Resistant
**Excess mineralocorticoid activity leads to same cascade as above
***No hypovolemia so urine chloride is generally normal (>10)

==DDX==
#Chloride-Responsive (urine Cl < 20 mEq/L)
##Loss of gastric secretions
###vomiting
###NG suction
###bulemia
##Loss of colonic secretions
###congenital chloridorrhea
###villous adenoma
##Thiazides/loop after D/C
##Post hypercapnia
##Cystic fibrosis
#Chloride-resistant (urine Cl > 20 mEq/L)
##With HTN
###Primary hyperaldo
####adrenal adenoma
####bilateral adrenal
####hyperplasia
####adrenal carcinoma
###11B-HSD2
####genetic, licorice
####chewing tobacco
####carbenoxolone
###CAH (11-Hydroxylase or 17-hydroxylase deficiency)
###Current diuretics + HTN
###Cushing syndrome
###Exogenous steroids
###Liddle syndrome
###Renovascular HTN
##Without HTN
###Bartter syndrome^
###Gitelman syndrome^
###Severe K+ depletion
###Current thiazides/loop
###Hypomagnesemia
#Other causes
##Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids)
##Milk alkali syndrome
##Hypercalcemia (inability to concentrate urine leads to hypovolemia)
##Intravenous penicillin
##Refeeding alkalosis
##Massive blood transfusion

^in children

==Treatment==
#Correct volume depletion
##Normal Saline
###Repletion of extracellular volume decr need for Na reaborption
###Delivery of Cl to distal tubule increases Cl/bicarb exchange
#Correct potassium depletion
##Giving K+ leads to movement of H+ out of cells -> acidosis
##Giving K+ stops hypokalemia-induced distal H+/K+ pump
#Correct chloride depletion
##Must give a reabsorbable anion to replace HCO3
#Correct mineralocorticoid excess
##Aldostorone antagonists if indicated (i.e. spironolactone)

*Note: if pt is edematous (CHF, cirrhosis), do NOT give NS
**If pt is hypokalemic KCl will correct both hypoK AND alkalosis

==Source ==
Emedicine, Tintinalli, UpToDate, Kaji 2011

[[Category:FEN]]
[[Category:Tox]]

Respiratory acidosis

2011-08-02T20:37:19Z

Ghasek:

==Background==
*acidemia = pH < 7.38
*respiratory acidosis = pCO2 > 42
*Acute respiratory acidosis: Change in pH = 0.008 X (40 - PaCO2)
vs. Chronic respiratory acidosis: Change in pH = 0.003 X (40 - PaCO2)
*determine if another primary acid/base disturbance is occurring
**calculate AG
**if HCO3 < 24 + (pCO2-40)/10 x 3(+/-1) then there is a superimposed primary metabolic acidosis
***for every 10mm increase in pCO2 >40, HCO3expected increases by 2-4mEq (2 if acute/limited time for metabolic compensation, 4 if chronic i.e. COPD)
**if HCO3 > 24 + (pCO2-40)/10 x 3(+/-1) then suspect primary metabolic alkalosis

==Etiology==
Hypoventilation - acute vs chronic

==DDX==
#COPD
#Drugs (opioids)
#Chest wall dz
#Pleural dz
#Trauma

==Treatment==
#Improve alveolar ventilation
##Bronchodilators
##CPAP
##Intubation (esp of pH < 7.25)
###Do not reduce pH too quickly (>5Hg/h)
####Can lead to abrupt hypocalcemia/hypokalemia

==Source ==
Tintinalli, KAJI 2011

[[Category:FEN]]
[[Category:Pulm]]
[[Category:Tox]]

Respiratory acidosis

2011-08-02T20:37:05Z

Ghasek:

Respiratory acidosis

2011-08-02T20:36:22Z

Ghasek:

==Background==
*acidemia = pH < 7.38
*respiratory acidosis = pCO2 > 42
*Acute respiratory acidosis: Change in pH = 0.008 X (40 - PaCO2)
Chronic respiratory acidosis: Change in pH = 0.003 X (40 - PaCO2)
*determine if another primary acid/base disturbance is occurring
**calculate AG
**if HCO3 < 24 + (pCO2-40)/10 x 3(+/-1) then there is a superimposed primary metabolic acidosis
***for every 10mm increase in pCO2 >40, HCO3expected increases by 2-4mEq (2 if acute/limited time for metabolic compensation, 4 if chronic i.e. COPD)
**if HCO3 > 24 + (pCO2-40)/10 x 3(+/-1) then suspect primary metabolic alkalosis

==Etiology==
Hypoventilation - acute vs chronic

==DDX==
#COPD
#Drugs (opioids)
#Chest wall dz
#Pleural dz
#Trauma

==Treatment==
#Improve alveolar ventilation
##Bronchodilators
##CPAP
##Intubation (esp of pH < 7.25)
###Do not reduce pH too quickly (>5Hg/h)
####Can lead to abrupt hypocalcemia/hypokalemia

==Source ==
Tintinalli, KAJI 2011

[[Category:FEN]]
[[Category:Pulm]]
[[Category:Tox]]

Respiratory acidosis

2011-08-02T20:33:51Z

Ghasek:

==Background==
*acidemia = pH < 7.38
*respiratory acidosis = pCO2 > 42
*determine if another primary acid/base disturbance is occurring
**calculate AG
**if HCO3 < 24 + (pCO2-40)/10 x 3(+/-1) then there is a superimposed primary metabolic acidosis
***for every 10mm increase in pCO2 >40, HCO3expected increases by 2-4mEq (2 if acute/limited time for metabolic compensation, 4 if chronic i.e. COPD)
**if HCO3 > 24 + (pCO2-40)/10 x 3(+/-1) then suspect primary metabolic alkalosis

==Etiology==
Hypoventilation - acute vs chronic

==DDX==
#COPD
#Drugs (opioids)
#Chest wall dz
#Pleural dz
#Trauma

==Treatment==
#Improve alveolar ventilation
##Bronchodilators
##CPAP
##Intubation (esp of pH < 7.25)
###Do not reduce pH too quickly (>5Hg/h)
####Can lead to abrupt hypocalcemia/hypokalemia

==Source ==
Tintinalli, KAJI 2011

[[Category:FEN]]
[[Category:Pulm]]
[[Category:Tox]]

Respiratory acidosis

2011-08-02T20:32:16Z

Ghasek:

Respiratory alkalosis

2011-08-02T20:30:44Z

Ghasek:

==Background==
*alkalemia = pH >7.42
*respiratory alkalosis = pCO2 <38
*Cause = hyperventilation
*May lead to hypocalcemia, hypokalemia
*Check for a concurrent acid/base disturbance
**always check for an AG
**for every 10mm pCO2 <40, HCO3 expected to decrease by 1-3.5 mEq
**if HCO3 < 24 - (40-pCO2)/10 x 2.5 (+/-1) then there is a superimposed primary metabolic acidosis
**if HCO3 > 24 - (40-pCO2)/10 x 2.5 (+/-1) then there is a primary metabolic alkalosis, or acute respiratory alkalosis without time for metabolic compensation

==DDX==
#Asthma
#PE
#DKA
#Anxiety
#Hypoxia
#early sepsis/fever/pneumonia
#Hyperthyroid
#Sympathomimetics
#[[Aspirin (Salicylate) Toxicity]]
#Progesterone/pregnancy
#Liver dz
#CVA or other central cause

==Source ==
KAJI 2011
Tintinalli, Kaji 2011

[[Category:FEN]]
[[Category:Pulm]]
[[Category:Tox]]

Respiratory acidosis

2011-08-02T19:39:56Z

Ghasek:

==Background==
*acidemia = pH < 7.38
*respiratory acidosis = pCO2 > 42
*determine if another primary acid/base disturbance is occurring
**calculate AG
**if HCO3 < 24 + (pCO2-40)/10 x 4 then there is a superimposed primary metabolic acidosis
***for every 10mm increase in pCO2 >40, HCO3expected increases by 2-4mEq (2 if acute/limited time for metabolic compensation, 4 if chronic i.e. COPD)
**if HCO3 > 24 + (pCO2-40)/10 x 4 then suspect primary metabolic alkalosis

==Etiology==
Hypoventilation - acute vs chronic

==DDX==
#COPD
#Drugs (opioids)
#Chest wall dz
#Pleural dz
#Trauma

==Treatment==
#Improve alveolar ventilation
##Bronchodilators
##CPAP
##Intubation (esp of pH < 7.25)
###Do not reduce pH too quickly (>5Hg/h)
####Can lead to abrupt hypocalcemia/hypokalemia

==Source ==
Tintinalli

[[Category:FEN]]
[[Category:Pulm]]

Metabolic acidosis

2011-08-02T19:16:40Z

Ghasek:

== Background ==
*Primary acidosis if pH <7.38
*HCO3 <24 = metabolic acidosis
*Always determine if there is another acid/base process occurring
**Primary respiratory acidosis if pCO2 > pCO2expected
**Primary respiratory alkalosis if pCO2 < pCO2expected
***use Winter's formula: PCO2 (expected) = (1.5 x [HCO3–] + 8) ± 2
***In acute setting PCO2 should fall by 1 mmHg for every 1 mEq fall in HCO3
**Concurrent metabolic alkalosis if delta-delta > 28
**Delta-Delta = (AG - 12) + HCO3

== DDX ==
=== Gap ===

#Lactic acidosis
##Sepsis, shock, liver dz, CO, CN, metformin, methemoglobin
#Renal failure
##Uremia
#Ketoacidosis
##DKA, AKA, starvation
#Ingestions
##Inc osm gap
###Methanol, ethylene glycol
##Normal osm gap
###ASA, iron, INH
##Osm gap = measured osm - calculated osm (normal 10-15)
##Calculated Osm = 2(Na)+(glucose/18)+(BUN/2.8)+(BAL/5)

=== Non-gap ===
#Hyperkalemia
##Resolving DKA
##Early uremic acidosis
##Early obstructive uropathy
##RTA Type IV
##Hypoaldo
##K-sparing diuretics
#Hypokalemia
##RTA Type I
##RTA Type II
##Acetazolamide
##Acute diarrhea
###(May be assoc with gap if hypoperfusion -> lactic acidosis)

== Treatment ==
#Treat source
#Correct any respiratory acidosis
#Bicarbonate
##HCO3 dose in mEq = 0.5(wt in kg) x (24 - measured HCO3)
##Each bicarb 0.5mEq/kg causes 1 meq/L rise in HCO3
##Consider for:
###Bicarb <4
###pH <7.20 AND shock/myocardial irritability
###Severe hyperchloremic acidemia
###lower threshold with non-AG acidosis (greater HCO3 loss)
####Lost bicarbonate would take days to replenish

== Source ==
Tintinalli
Kaji 2011

[[Category:FEN]]
[[Category:Tox]]

Metabolic acidosis

2011-08-02T19:11:02Z

Ghasek:

== Background ==
*Primary acidosis if pH <7.38
*HCO3 <24 = metabolic acidosis
*Always determine if there is another acid/base process occurring
**Primary respiratory acidosis if pCO2>pCO2expected - use Winter's formula
***PCO2 (expected) = (1.5 x [HCO3–] + 8) ± 2
***In acute setting PCO2 should fall by 1 mmHg for every 1 mEq fall in HCO3
**Concurrent metabolic alkalosis if delta-delta > 28
**Delta-Delta = (AG - 12) + HCO3

== DDX ==
=== Gap ===

#Lactic acidosis
##Sepsis, shock, liver dz, CO, CN, metformin, methemoglobin
#Renal failure
##Uremia
#Ketoacidosis
##DKA, AKA, starvation
#Ingestions
##Inc osm gap
###Methanol, ethylene glycol
##Normal osm gap
###ASA, iron, INH
##Osm gap = measured osm - calculated osm (normal 10-15)
##Calculated Osm = 2(Na)+(glucose/18)+(BUN/2.8)+(BAL/5)

=== Non-gap ===
#Hyperkalemia
##Resolving DKA
##Early uremic acidosis
##Early obstructive uropathy
##RTA Type IV
##Hypoaldo
##K-sparing diuretics
#Hypokalemia
##RTA Type I
##RTA Type II
##Acetazolamide
##Acute diarrhea
###(May be assoc with gap if hypoperfusion -> lactic acidosis)

== Treatment ==
#Treat source
#Correct any respiratory acidosis
#Bicarbonate
##HCO3 dose in mEq = 0.5(wt in kg) x (24 - measured HCO3)
##Each bicarb 0.5mEq/kg causes 1 meq/L rise in HCO3
##Consider for:
###Bicarb <4
###pH <7.20 AND shock/myocardial irritability
###Severe hyperchloremic acidemia
###lower threshold with non-AG acidosis (greater HCO3 loss)
####Lost bicarbonate would take days to replenish

== Source ==
Tintinalli
Kaji 2011

[[Category:FEN]]
[[Category:Tox]]

Metabolic alkalosis

2011-08-02T18:49:49Z

Ghasek:

==Background==
*pH > 7.42 = alkalemia
*HCO3 > 28 = metabolic alkalosis
*Always determine if there is also a concurrent primary respiratory process
**expected pCO2 = 40 + 0.6(measured HCO3 - 24)
**if pCO2>pCO2 expected, then there is also a primary respiratory acidosis
**if pCO2<pCO2 expected, then there is also primary respiratory alkalosis

==Pathophysiology==
*Chloride-Responsive (volume depletion)
**Condition that produces chloride loss also tends to reduce extracellular volume
***Reduction in extracellular volume increases mineralocorticoid activity
****Enhances Na reabsorption and K+/H+ secretion in renal tubule
*****K/H+ secretion -> HCO3 generation
******Resulting urine is alkaline with little chloride (<10)
*Chloride-Resistant
**Excess mineralocorticoid activity leads to same cascade as above
***No hypovolemia so urine chloride is generally normal (>10)

==DDX==
#Chloride-Responsive (urine Cl < 20 mEq/L)
##Loss of gastric secretions
###vomiting
###NG suction
###bulemia
##Loss of colonic secretions
###congenital chloridorrhea
###villous adenoma
##Thiazides/loop after D/C
##Post hypercapnia
##Cystic fibrosis
#Chloride-resistant (urine Cl > 20 mEq/L)
##With HTN
###Primary hyperaldo
####adrenal adenoma
####bilateral adrenal
####hyperplasia
####adrenal carcinoma
###11B-HSD2
####genetic, licorice
####chewing tobacco
####carbenoxolone
###CAH (11-Hydroxylase or 17-hydroxylase deficiency)
###Current diuretics + HTN
###Cushing syndrome
###Exogenous steroids
###Liddle syndrome
###Renovascular HTN
##Without HTN
###Bartter syndrome^
###Gitelman syndrome^
###Severe K+ depletion
###Current thiazides/loop
###Hypomagnesemia
#Other causes
##Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids)
##Milk alkali syndrome
##Hypercalcemia (inability to concentrate urine leads to hypovolemia)
##Intravenous penicillin
##Refeeding alkalosis
##Massive blood transfusion

^in children

==Treatment==
#Correct volume depletion
##Normal Saline
###Repletion of extracellular volume decr need for Na reaborption
###Delivery of Cl to distal tubule increases Cl/bicarb exchange
#Correct potassium depletion
##Giving K+ leads to movement of H+ out of cells -> acidosis
##Giving K+ stops hypokalemia-induced distal H+/K+ pump
#Correct chloride depletion
##Must give a reabsorbable anion to replace HCO3
#Correct mineralocorticoid excess
##Aldostorone antagonists if indicated (i.e. spironolactone)

*Note: if pt is edematous (CHF, cirrhosis), do NOT give NS
**If pt is hypokalemic KCl will correct both hypoK AND alkalosis

==Source ==
Emedicine, Tintinalli, UpToDate, Kaji 2011

[[Category:FEN]]
[[Category:Tox]]

Metabolic alkalosis

2011-08-02T18:41:25Z

Ghasek:

==Pathophysiology==
*Chloride-Responsive (volume depletion)
**Condition that produces chloride loss also tends to reduce extracellular volume
***Reduction in extracellular volume increases mineralocorticoid activity
****Enhances Na reabsorption and K+/H+ secretion in renal tubule
*****K/H+ secretion -> HCO3 generation
******Resulting urine is alkaline with little chloride (<10)
*Chloride-Resistant
**Excess mineralocorticoid activity leads to same cascade as above
***No hypovolemia so urine chloride is generally normal (>10)

==DDX==
#Chloride-Responsive (urine Cl < 20 mEq/L)
##Loss of gastric secretions
###vomiting
###NG suction
###bulemia
##Loss of colonic secretions
###congenital chloridorrhea
###villous adenoma
##Thiazides/loop after D/C
##Post hypercapnia
##Cystic fibrosis
#Chloride-resistant (urine Cl > 20 mEq/L)
##With HTN
###Primary hyperaldo
####adrenal adenoma
####bilateral adrenal
####hyperplasia
####adrenal carcinoma
###11B-HSD2
####genetic, licorice
####chewing tobacco
####carbenoxolone
###CAH (11-Hydroxylase or 17-hydroxylase deficiency)
###Current diuretics + HTN
###Cushing syndrome
###Exogenous steroids
###Liddle syndrome
###Renovascular HTN
##Without HTN
###Bartter syndrome^
###Gitelman syndrome^
###Severe K+ depletion
###Current thiazides/loop
###Hypomagnesemia
#Other causes
##Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids)
##Milk alkali syndrome
##Hypercalcemia (inability to concentrate urine leads to hypovolemia)
##Intravenous penicillin
##Refeeding alkalosis
##Massive blood transfusion

^in children

==Treatment==
#Correct volume depletion
##Normal Saline
###Repletion of extracellular volume decr need for Na reaborption
###Delivery of Cl to distal tubule increases Cl/bicarb exchange
#Correct potassium depletion
##Giving K+ leads to movement of H+ out of cells -> acidosis
##Giving K+ stops hypokalemia-induced distal H+/K+ pump
#Correct chloride depletion
##Must give a reabsorbable anion to replace HCO3
#Correct mineralocorticoid excess
##Aldostorone antagonists if indicated (i.e. spironolactone)

*Note: if pt is edematous (CHF, cirrhosis), do NOT give NS
**If pt is hypokalemic KCl will correct both hypoK AND alkalosis

==Source ==
Emedicine, Tintinalli, UpToDate, Kaji 2011

[[Category:FEN]]
[[Category:Tox]]

Metabolic alkalosis

2011-08-02T18:40:31Z

Ghasek:

==Pathophysiology==
*Chloride-Responsive (volume depletion)
**Condition that produces chloride loss also tends to reduce extracellular volume
***Reduction in extracellular volume increases mineralocorticoid activity
****Enhances Na reabsorption and K+/H+ secretion in renal tubule
*****K/H+ secretion -> HCO3 generation
******Resulting urine is alkaline with little chloride
*Chloride-Resistant
**Excess mineralocorticoid activity leads to same cascade as above
***No hypovolemia so urine chloride is generally normal

==DDX==
#Chloride-Responsive (urine Cl < 20 mEq/L)
##Loss of gastric secretions
###vomiting
###NG suction
###bulemia
##Loss of colonic secretions
###congenital chloridorrhea
###villous adenoma
##Thiazides/loop after D/C
##Post hypercapnia
##Cystic fibrosis
#Chloride-resistant (urine Cl > 20 mEq/L)
##With HTN
###Primary hyperaldo
####adrenal adenoma
####bilateral adrenal
####hyperplasia
####adrenal carcinoma
###11B-HSD2
####genetic, licorice
####chewing tobacco
####carbenoxolone
###CAH (11-Hydroxylase or 17-hydroxylase deficiency)
###Current diuretics + HTN
###Cushing syndrome
###Exogenous steroids
###Liddle syndrome
###Renovascular HTN
##Without HTN
###Bartter syndrome^
###Gitelman syndrome^
###Severe K+ depletion
###Current thiazides/loop
###Hypomagnesemia
#Other causes
##Exogenous alkali (Nabicarb + renal failure, metabolism of lactic acid, or ketoacids)
##Milk alkali syndrome
##Hypercalcemia (inability to concentrate urine leads to hypovolemia)
##Intravenous penicillin
##Refeeding alkalosis
##Massive blood transfusion

^in children

==Treatment==
#Correct volume depletion
##Normal Saline
###Repletion of extracellular volume decr need for Na reaborption
###Delivery of Cl to distal tubule increases Cl/bicarb exchange
#Correct potassium depletion
##Giving K+ leads to movement of H+ out of cells -> acidosis
##Giving K+ stops hypokalemia-induced distal H+/K+ pump
#Correct chloride depletion
##Must give a reabsorbable anion to replace HCO3
#Correct mineralocorticoid excess
##Aldostorone antagonists if indicated (i.e. spironolactone)

*Note: if pt is edematous (CHF, cirrhosis), do NOT give NS
**If pt is hypokalemic KCl will correct both hypoK AND alkalosis

==Source ==
Emedicine, Tintinalli, UpToDate, Kaji 2011

[[Category:FEN]]
[[Category:Tox]]

Metabolic acidosis

2011-08-02T18:24:58Z

Ghasek:

== Background ==
*Primary acidosis if pH <7.38
*HCO3 <24 = metabolic acidosis
*Always determine whether there is a primary respiratory acidosis as well (Winter's formula)
**PCO2 (expected) = (1.5 x [HCO3–] + 8) ± 2
**In acute setting PCO2 should fall by 1 mmHg for every 1 mEq fall in HCO3

== DDX ==
=== Gap ===

#Lactic acidosis
##Sepsis, shock, liver dz, CO, CN, metformin, methemoglobin
#Renal failure
##Uremia
#Ketoacidosis
##DKA, AKA, starvation
#Ingestions
##Inc osm gap
###Methanol, ethylene glycol
##Normal osm gap
###ASA, iron, INH
##Osm gap = measured osm - calculated osm (normal 10-15)
##Calculated Osm = 2(Na)+(glucose/18)+(BUN/2.8)+(BAL/5)

=== Non-gap ===
#Hyperkalemia
##Resolving DKA
##Early uremic acidosis
##Early obstructive uropathy
##RTA Type IV
##Hypoaldo
##K-sparing diuretics
#Hypokalemia
##RTA Type I
##RTA Type II
##Acetazolamide
##Acute diarrhea
###(May be assoc with gap if hypoperfusion -> lactic acidosis)

== Treatment ==
#Treat source
#Correct any respiratory acidosis
#Bicarbonate
##HCO3 dose in mEq = 0.5(wt in kg) x (24 - measured HCO3)
##Each bicarb 0.5mEq/kg causes 1 meq/L rise in HCO3
##Consider for:
###Bicarb <4
###pH <7.20 AND shock/myocardial irritability
###Severe hyperchloremic acidemia
###lower threshold with non-AG acidosis (greater HCO3 loss)
####Lost bicarbonate would take days to replenish

== Source ==
Tintinalli
Kaji 2011

[[Category:FEN]]
[[Category:Tox]]

Metabolic acidosis

2011-08-02T18:08:20Z

Ghasek:

== Background ==
*Primary acidosis if pH <7.38
*HCO3 <24 = metabolic acidosis
*Always determine whether there is a primary respiratory acidosis as well
**PCO2 (expected) = (1.5 x [HCO3–] + 8) ± 2
**In acute setting PCO2 should fall by 1 mmHg for every 1 mEq fall in HCO3

== DDX ==
=== Gap ===

#Lactic acidosis
##Sepsis, shock, liver dz, CO, CN, metformin, methemoglobin
#Renal failure
##Uremia
#Ketoacidosis
##DKA, AKA, starvation
#Ingestions
##Inc osm gap
###Methanol, ethylene glycol
##Nl osm gap
###Salicylates

=== Non-gap ===
#Hyperkalemia
##Resolving DKA
##Early uremic acidosis
##Early obstructive uropathy
##RTA Type IV
##Hypoaldo
##K-sparing diuretics
#Hypokalemia
##RTA Type I
##RTA Type II
##Acetazolamide
##Acute diarrhea
###(May be assoc with gap if hypoperfusion -> lactic acidosis)

== Treatment ==
#Treat source
#Correct any respiratory acidosis
#Bicarbonate
##Each bicarb 0.5mEq/kg causes 1 meq/L rise in HCO3
##Consider for:
###Bicarb <4
###pH <7.20 AND shock/myocardial irritability
###Severe hyperchloremic acidemia
####Lost bicarbonate would take days to replenish

== Source ==
Tintinalli
Kaji 2011

[[Category:FEN]]
[[Category:Tox]]