Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine (36 page)

Fluids & vasoactive drugs

•
Early goal-directed therapy
(“Rivers Protocol,”
NEJM
2001;345:1368), confirm. trials pending

Insert arterial & central venous lines (
NEJM
2007;356:e21; PAC not needed) and ✓ MAP, CVP & S
_cv
O
₂
(central venous O
₂
sat, nl 60–80%) which measures O
₂
consumption vs. delivery (less invasive than mixed venous) w/ low S
_CV
O
₂
→ ↓ O
₂
delivery (↓ S
_a
O
₂
, nl S
_a
O
₂
but ↓ CO or anemia) or excessive O
₂
consumption

Target MAP ≥65 mmHg, CVP 8–12 mmHg, & UOP ≥0.5 mL/kg/h using fluid (eg, 500 mL NS q30min) and vasopressors as needed

Target S
_cv
O
₂
≥70% using PRBCs & inotropes (dobutamine, ↑ dose as needed q15min)

When done w/in first 6 h for severe sepsis & septic shock, 42% ↓ mortality

• Lactate clearance (≥20% / 2 h) as effective as S
_cv
O
₂
to guide resuscitation (
  JAMA
2010;303:739) • Crystalloid better than colloid for resuscitation (
NEJM
2004;350:2247 & 2012;367:124 & 1901) • Norepi ↓ arrhyth. & mort. c/w dopamine (
NEJM
2010;362:779;
Crit Care Med
2012;40:725) • Vasopressin added to low-dose norepinephrine not superior to high-dose norepinephrine (
NEJM
2008;358:877); consider if HoTN refractory to catecholamine vasopressors • Use PRBC w/ caution, may ↑ mortality/morbidity, ↑ risk of ARDS (
Crit Care Med
2005;33:1191); ∴ goal Hb 7 unless active cardiac ischemia (
NEJM
1999;340:409) • After early resuscitation, if ALI/ARDS, target CVP 4–6 mmHg as additional fluids may be harmful → ↑ ventilator/ICU days (
NEJM
2006;354:2564;
Chest
2008;133:252) • Pulse pressure variation >13% with respiration → likely volume-responsive (
Chest
2008;133:252); only validated in passive, intubated Pts and studied in higher tidal volumes
Antibiotics

• Start empiric IV abx w/in 1 h of recognition of severe sepsis or septic shock; every hour delay in abx admin a/w 8% ↑ in mortality (
Crit Care Med
2006;34:1589) • If possible, obtain 2 sets of BCx before urgently starting abx (but do not delay abx) • Typically want broad gram-positive and gram-negative coverage, including MRSA and highly resistant gram-negative bacilli ± anaerobes
Steroids
(
NEJM
2003;348:727;
JAMA
2009;301:2362)

• Cortisol secretion helps predict mortality, but treatment of adrenal insufficiency is unproven (
  JAMA
2000;283:1038;
NEJM
2008;358:111) • Earlier study showed
possible
mortality benefit w/in 8 h of severe septic shock (SBP <90 for >1 h despite fluids & pressors) if post ACTH stim cortisol Δ ≤ 9 µg/dL (
  JAMA
2002;288:862) • No mortality benefit to early (<72 h) empiric corticosteroids in all Pts w/ septic shock, regardless of ACTH stim; faster resolution of shock, more superinfection (
NEJM
2008;358:111) • ? hydrocortisone 50–100 q6–8h ± fludrocortisone 50 µg daily in septic shock refractory to fluids & pressors, regardless of ACTH stim (
Crit Care Med
2008;36:296)
Activated protein C

• No longer FDA approved, no improvement in mortality (
NEJM
2012;366:2055)
Intensive glycemic control
(
NEJM
2010;363:2540)

• No evidence of improved outcomes in MICU population w/ intensive glycemic control • Intensive glycemic control to goal 80–110 mg/dL in
surgical
ICU population → mortality benefit, greatest if >3-d ICU stay (
NEJM
2001;345:1359) • Repeat studies suggest intensive glycemic control → either no Δ or ↑ increased mortality, and definite ↑ hypoglyc. (
  JAMA
2008;300:933;
NEJM
2006;354:449; 2008;358:125; 2009;360:1283) • Hypoglycemia associated with mortality (
NEJM
2012;367:1108) • Reasonable to keep glc <150 mg/dL in severe sepsis, using validated protocol (
Crit Care Med
2008;36:296)

NOTES

ESOPHAGEAL AND GASTRIC DISORDERS

DYSPHAGIA

Definitions

• Oropharyngeal: inability to propel food from mouth through UES into esophagus • Esophageal: difficulty swallowing & passing food from esophagus into stomach

Figure 3-1 
Etiologies of and approach to dysphagia (
NCP Gastrohep
2008;5:393;
Neurogastro
2012;24:57)

Achalasia

• Etiologies: idiopathic (most common), pseudoachalasia (due to GE jxn tumor), Chagas • Sx: dysphagia (solid & liquid), chest pain (
¹
/
₃
of Pts), regurgitation • Dx: barium swallow → dilated esophagus w/ distal “bird’s beak” narrowing; manometry → simultaneous, low amplitude contractions of esophageal body, incomplete relaxation of lower esophageal sphincter (± LES hypertension); EGD → r/o pseudoachalasia (retroflex) • Rx: expert pneumatic dilation (≤4% eso perf)
lap Heller myotomy (
NEJM
2011;364:1868)
Other esophageal disorders

• Webs (upper/mid esoph; congenital, GVHD, Fe-defic anemia); Rings (lower; ? due to GERD); Zenker’s diverticulum (pharyngoesoph jxn); dx w/ barium swallow; Rx: endo/surg • Infxn esophagitis: odynophagia > dysphagia; often immunosupp w/
Candida
, HSV, CMV

• Pill esophagitis: odynophagia > dysphagia; NSAID, KCl, bisphosp., doxy & tetracycline • Eosinophilic esophagitis (
Clin Gastro & Hep
2012;10:1066): seen in young or middle-aged, predom
. Dx req >15 eos/hpf on bx & exclude GERD (eg, empiric PPI trial). Rx: 3
D
s:
D
iet (elim milk, soy, eggs, wheat, nuts, fish);
D
rugs (swallow inh steroids),
D
ilation

GASTROESOPHAGEAL REFLUX DISEASE (GERD)

Pathophysiology

• Excessive transient relaxations of lower esophageal sphincter (LES) or incompetent LES

• Mucosal damage (esophagitis) due to prolonged contact w/ acid can evolve to stricture • Risk factors: hiatal hernia, obesity, gastric hypersecretory states, delayed emptying • Precipitants: supine position, fatty foods, caffeine, alcohol, cigarettes, CCB, pregnancy
Clinical manifestations

• Esophageal:
heartburn
, atypical chest pain, regurgitation, water brash, dysphagia • Extraesophageal:
cough
, asthma (often poorly controlled), laryngitis, dental erosions
Diagnosis
(
Gastro
2008;135:1383;
Am J Gastro
2010;105:747;
Annals
2012;157:808)
• Based on hx & empiric trial of PPI (Se & Sp: 78% & 54%) (
Annals
2004;140:518) • EGD if: (1) failure to respond to bid PPI; (2)
alarm features
: dysphagia, vomiting, wt loss, evid of blood loss; or ? (3)
>50 y w/ sx ≥5 y + nocturnal sx, hiatal hernia, obesity, cigs • If dx uncertain & EGD nl → high res manometry w/ 24-h esoph pH monitoring ± impedance
Treatment
(
NEJM
2008;359:1700)
• Lifestyle: avoid precipitants, lose weight, avoid large & late meals, elevate head of bed • Medical: PPI achieve relief in 80–90% (titrate to lowest dose that achieves sx control)
surgery among Pts who initially respond to acid suppression (
JAMA
2011;305:1969) • Refractory: confirm w/ pH testing: if acidic or sx correlate w/ reflux episodes → surgical fundoplication (implantation of magnetic esophageal sphincter device being studied;
NEJM
2013;368:719); if nl pH or no sx correlation → TCA, SSRI or baclofen (
Gastro
2010;139:7.e3)
Complications
(
NEJM
2009;361:2548;
Gastro
2011;140:1084 & e18)
• Barrett’s esophagus: dx by bx of intestinal metaplasia above GE jxn. Screen for BE if ≥2 of the following risk factors: >50 y, male, white, chronic GERD, hiatal hernia, high BMI.