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96
Hypothalamus
Hypothalamus
Physiological situation Primary adrenal insufficiency
Pituitary disease Hypothalamic disease
https://t.me/medicina_free
Hypothalamus
CRH
Pituitary
ACTH
Adrenal
Secondary adrenal insufficiency
CRH↑
Pituitary
ACTH↓
Adrenal
CRH↑
Pituitary
ACTH↑
Adrenal
Cortisol
Hypothalamus
Pituitary
Adrenal
Cortisol↓ Cortisol↓
Cortisol↓
CRH↓
ACTH↓
Figure11.3 Primar y and secondary adrenal insufciency.
CRH=corticotropin- releasing hormone SOURCE:Reprinted
from The Lancet 2003 May 31;361(9372):1881- 93. Arlt W, Allolio
B.:Adrenal insufciency, with permission from Elsevier
cause of shock? Describe clinical signs that would lead
you to diagnose distributiveshock.
3. How do hepatitis C and the potential for hepatic
cirrhosis aect the presentation and course of septic
shock? Does this aect your choice of intervention and
choice of rst- line antibiotics?
4. What further testing would you initiate before starting
treatment of this patient? How would you assess the
adequacy of perfusion? Would you place a central
venous catheter and/ or arterial catheter?Why?
5. How would you monitor the success of uid
resuscitation? Central venous pressure? Central venous
oxygenation? Arterial lactate concentrations? Urine
output? How does hepatic cirrhosis aect these variables?
6. e patient remains hypotensive with low urine output 2
hours aer uid administration. What is your dierential
diagnosis at this time? Does the presence of hepatic
cirrhosis aect the responsiveness to resuscitation? What
vasopressor would you start, andwhen?
7. How do you assess whether the liver function is
adequate? Can we rule out signicant liver dysfunction
if the conventional liver function tests are normal? How
does cirrhosis aect outcome in patients with sepsis?
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181. Millis JM, Melinek J, Csete M, etal. Randomized controlled trial
to evaluate ush and reperfusion techniques in liver transplantation. Transplantation 1997;63:397–403.
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Eects of atropine pretreatment on the revascularization syndrome. Transplantation proceedings 1989;21:2341–2.
184. Pittet JF, Morel DR, Mentha G, Le Coultre C, Suter PM, Rohner
A. Protective eect of indomethacin in the development of the
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G. Epidemiology of life- threatening and lethal anaphylaxis: a
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186. Simon MR, Mulla ZD. A population- based epidemiologic analysis
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histamine:analysis of the eects of H- 1 and H- 2 histamine receptor antagonists on cardiovascular and pulmonary responses. e
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188. Sampson HA, Munoz- Furlong A, Campbell RL, etal. Second symposium on the denition and management of anaphylaxis: summary report- - Second National Institute of Allergy and Infectious
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England journal of medicine 1992;327:380–4.
190. omas M, Crawford I. Best evidence topic report. Glucagon infusion in refractory anaphylactic shock in patients on beta- blockers.
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F. Addison disease in patients treated with glucocorticoid therapy.
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196. Grossman A, Johannsson G, uinkler M, Zelissen P. erapy of
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G. Premature mortality in patients with Addison’s disease: a
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metabolism 2006;91:4849–53.
DISTRIBUTIVESHOCK 101
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EBVHct Hct
if
av
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12.
HYPOVOLEMICSHOCK
Paul David Weyker, Christopher Allen- John Webb, and Tricia E. Brentjens
CASE
BOX 12.1 ESTIMATED ALLOWABLE BLOOD LOSS(EABL)
A 23- year- old woman G3P2 at 40 weeks gestation presents
for a planned tertiary cesarean section. Aprior ultrasound
showed placenta previa with suspected placenta accreta. An
expired type and screen was found to have antibodies. e
preoperative nurse has already placed one 18G intravenous
catheter. Her vital signs are within normal limits, and her
hemoglobin level is 9.5 g/ dL, platelet count 350 × 109/ L,
and coagulation studies are within normal limits. e
obstetrician tells you that she is “concerned” this will be a
ABL
=
EBV=Estimated Blood Volume of the patient
Hcti=Patient’s Initial Hematocrit
Hctf=Minimal Allowable Hematocrit for your patient
Hctav=Average of Hcti andHct
Reference:Estimating Allowable Blood Loss:Corrected for Dilution. Jeffrey B Gross.
Anesthesiology,1983.
Hct
f
dicultcase.
INTRODUCTION
pressure variation (PPV), systolic pressure variation (SPV),
and stroke volume variation (SVV) into perioperative mon-
itoring systems, many clinicians are able to follow trends in
Broadly dened, hypovolemia represents inadequate circulating plasma volume leading to decreased cardiac preload
and thus decreased blood pressure. Common causes of hypovolemic shock during the perioperative period include hemorrhage, diuretics, and gastrointestinal losses. Preoperative
assessment of volume status determines whether the patient
is relatively hypovolemic. e anesthetic plan includes calculation of allowable blood loss (Box 12.1 and Table 12.1).1
e anesthesiologist should ask about conditions that may
predispose the patient to hypovolemia such as diuretic use,
these dynamic measurements to predict uid responsive-
ness in mechanically ventilated patients. Models of sepsis-
induced hypotension have demonstrated that both SPV2
and PPV3 are sensitive markers for predicting uid respon-
siveness. Central venous pressure (CVP) is a poor monitor
for hypovolemia, because values are highly variable and are
inuenced by venous compliance, pleural pressure, abdom-
inal pressure, and intravascular volume.4 Central venous
pressure is best used as a trend monitor in cases of right
heart failure and aer open- heart surgery.
prolonged NPO status, vomiting, or diarrhea. Prompt
resuscitation is imperative to restore blood ow and thus
oxygen delivery to tissues. Volume decits can be replaced
DIURETIC- INDUCED HYPOVOLEMIA
with crystalloid, colloid, or blood products.
Diuretics are among the most commonly used antihyper-
HEMODYNAMIC MONITORING
FORHYPOVOLEMIA
tensive medications in the world. Diuretics impair renal
reabsorption of solutes to decrease reabsorption of water.
In general, diuretics are classied based on their location of
action within the nephron, and specic diuretics are associIn recent years, an emphasis on goal- directed uid therapy
has changed clinical practice in the perioperative setting.
With the introduction of dynamic monitors such as pulse
ated with dierent electrolyte abnormalities (Table 12.2).5
Consensus on whether or not to hold diuretics on the day
of surgery is lacking, and this decision oen varies among
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TABLE12.1 EBV=WEIGHT (KG) × AVERAGE BLOODVOLUME
Blood Volume mL/ kg
Premature 95
Neonate 90
Infant 85
Adult Man 75
Adult Woman 65
of high volumes may cause a hyperchloremic metabolic acidosis. e SAFE trial, a multicenter, randomized, doubleblind, trial of nearly 7,000 patients compared the use of
albumin versus normal saline for uid resuscitation in the
intensive care unit (ICU). is trial found no signicant
dierence in 28- day mortality.6 e CRISTAL trial was a
large multicenter, randomized trial comparing the use of
colloids versus crystalloids for resuscitation in 2,857 ICU
patients with hypovolemic shock. Patients were randomized to receive either colloids (gelatins, dextrans, hydroxy-
ethyl starches, or albumin) or crystalloids (normal saline or
dierent institutions. Obtaining a history about diuretic
use and evaluation of electrolyte abnormalities can help
manage the patient’s perioperative uid status.
CRYSTALLOID VERSUS COLLOID
Ringer’s lactate solution) for all uid administration other
than maintenance uids in the ICU. is study found no
dierence in 28- day mortality, although there was a small
mortality benet in the colloid group at 90days.
7
HEMORRHAGE
Optimal resuscitation uid has been debated without any
clear consensus of mortality benets. Ageneral rule when
comparing the use of crystalloid versus colloid is that one
must give approximately 1.4– 1.6 times as much volume
of crystalloid as compared to colloid, due to extravascular
uid distribution of crystalloids. Crystalloids are much less
expensive compared to colloids, and for this reason, they
are oen the uid of choice in acute resuscitation of hypovolemic patients. Normal saline (NaCl) is oen the uid of
choice in acute volume resuscitation, but the administration
Hemorrhage is dened as the loss of blood from either
blood vessels or mucosal surfaces. While many classica-
tion systems for hemorrhage exist, perhaps the most widely
recognized classication is from the American College of
Surgeons. e Advanced Trauma Life Support (ATLS) sys-
tem classies patients into four main categories based on a
set of clinical signs obtained during the initial presentation
(heart rate, systolic blood pressure, pulse pressure, respira-
tory rate, mental status, and hourly urine output).8 Adult
TABLE12.2 COMMONLY USED DIURETICS
Diuretic
Loop (furosemide,
bumetanide, torsemide,
ethacrynic acid)
Thiazide
(hydrochlorothiazide,
chlorothiazide)
Potassiumsparing (amiloride,
triameterene,
spironolatone,
eplerenone)
Carbonic Anhydrase
Inhibitors
(Acetazolamide)
Osmotic Diuretics
(Mannitol)
Mechanism of Action Electrolyte Abnormalities
Blocks Na- K- ATPase in thick
ascending limb of loop of Henle
Sodium transport inhibition in distal
tubule
All work in cortical collecting tubule.
Spironolactone and eplerenone are
aldosterone antagonists, amiloride
and triameterene decrease sodium
channel activity
Primarily works in the proximal
tubule, carbonic anhydrase inhibitor
causing NaCl and bicarbonate loss
Nonreabsorbable sugar inhibiting
sodium and water reabsorption in the
proximal tubule and loop of Henle
Indications
hyponatremia, hypokalemia,
hypochloremia, hypomagnesemia,
hypocalcemia, metabolic alkalosis
hyponatremia, hypokalemia,
hypomagnesemia, hypochloremia,
hypercalcemia, metabolic alkalosis
hyperkalemia Spironolactone (CHF unresponsive to other
metabolic acidosis (decreases
serum bicarbonate)
hypernatremia or dilutional
hyponatremia, dilutional metabolic
acidosis, hyperosmolality induced
hyperkalemia
hypertension, heart failure edema, acute
pulmonary edema
hypertension, heart failure edema
therapies, hypokalemia, edema/ ascites
associated with cirrhosis, hypertension,
primary hyperaldosterionism) Amiloride
(used to counteract hypokalemia associated
with other diuretics
altitude sickness, edema, epilepsy,
glaucoma, metabolic alkalosis
reduction of increased intracranial pressure,
reduction of intraocular pressure, promoting
urinary excretion of toxic substances,
transurethral surgical procedures
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TABLE12.3 ATLS CLASS OFHEMORRHAGE
ClassI ClassII ClassIII
Blood loss (mL) Up to 750 750- 1500 1500- 2000 >2000
Blood loss (%blood volume) Up to 15% 15%- 30% 30%- 40% >40%
Pulse rate (BPM) <100 100- 120 120- 140 >140
Systolic blood pressure Normal Normal Decreased Decreased
Pulse pressure (mmHg) Normal or increased Decreased Decreased Decreased
Respiratory rate (per minute) 14- 20 20- 30 30- 40 >35
Urine output (mL/ hr) >30 20- 30 5- 15 Negligible
Central nervous system/
mental status
Initial uid replacement Crystalloid Crystalloid Crystalloid and Blood Crystalloid and Blood
SOURCE:Reprinted from the Advanced Trauma Life Support Student Course Manual, with permission of the American College of Surgeons.
Slightly anxious Mildly anxious Anxious, confused Confused, lethargic
patients can lose up to 30% of their circulating blood volume, ClassII hemorrhage, before having a decrease in blood
pressure (see Table 12.3). ClassII hemorrhage can rapidly
progress to ClassIII hemorrhage, where there is a 40% loss
early blood product administration.14 While the BD does
seem promising, larger, prospective studies are needed to
more clearly dene its role in risk stratication of patients
presenting with hemorrhagicshock.
ClassIV
in circulating blood volume along with signs of inadequate
perfusion, marked tachycardia, tachypnea, altered mental
status, decreased urine output, and decreased blood pressure.8 Based on the classication of hemorrhage, ATLS
PREOPERATIVE IDENTIFICATION OFPATIENTS
ATRISK FORBLEEDING
makes recommendations for initial uid replacement of
crystalloid +/ - blood.8 Derangements in cardiovascular
physiology are multifactorial, which makes it dicult to
apply the ATLS classication to every patient.
9,10
Arecent
retrospective study of over 36,000 trauma patients attempted
to classify patients based on heart rate, blood pressure, and
Glasgow coma scale. Over 90% of trauma patients were
unable to be correctly classied into the ATLS system for
hypovolemic shock.11 Other modalities have been investigated for the assessment of hypovolemic shock. Although
the concept of base decit (BD) as a surrogate for volume
decit is not new,12 there are few studies validating its use
for classifying hypovolemic shock. Davis and colleagues
initially described the four classes of hypovolemic shock
based on the BD of trauma patients.13 Severity of shock
was graded with a BD of 2– 6 mmol/ L, 6– 10 mmol/ L,
and greater than 10mmol/ L associated with mild, moderate, or severe shock, respectively.13 In order to validate this
new system in trauma patients, Mutschler etal. retrospectively applied the BD classication to over 16,000 trauma
patients.14 When compared with the traditional ATLS system, the BD classication was found to be superior not only
in identifying the presence of hypovolemic shock but also
in the early recognition of patients who may benet from
As part of the preoperative evaluation, anesthesiologists
identify patients at risk for signicant perioperative blood
loss. Both patient- and procedure- specic risk factors are
identied (Table 12.4). Patients with a previous history for
perioperative bleeding; known coagulopathies secondary
to medications or underlying disease states such as endstage liver disease, renal failure, or hemophilia; or patients
undergoing major vascular surgery, cardiac surgery with or
without cardiopulmonary bypass, or hepatic resection may
be at increased risk for perioperative bleeding. Adequate
intravenous access should be obtained in patients at high
risk of bleeding or who are undergoing surgical procedures
associated with a large amount of blood loss to ensure the
ability to quickly restore intravascular volume. Approximate
ow rates for intravenous catheters are shown in Table12.5.
Flow rate through a catheter is proportional to the radius to
the fourth power, and inversely proportional to the length
of the catheter, following the Hagen- Poiseuille equation. If
the radius of the catheter doubles, the ow rate increases by
a factor of 16. Aperipheral IV (5cm) will theoretically allow
three times the ow rate compared to the central venous
catheter (15cm) with the same gauge. For this reason, central catheters, due to their long length, are inadequate for
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TABLE12.4 PERIOPERATIVE FACTORS ASSOCIATED
WITHHEMORRHAGE
Patient Factors Surgical Factors
Drugs (aspirin, warfarin, etc.) Cardiopulmonar y bypass
Liver disease Liver transplant
Kidney disease ECMO
Thrombocytopenia Open major vascular surgery
Von Willebrand disease
Hemophilia
Sepsis
DIC
Vitamin K deciency
vessel and can be stopped with clamping or occlusion.15
TABLE12.5 ESTIMATED INTRAVENOUS
CATHETER FLOWRATES
Gauge
22 2.5cm 35
20 3.2cm 60
18 3.2cm 105
16 3.2cm 215
14 5.0cm 345
14 16cm 90
16 16cm 50
18 16cm 25
Length
Flow Rate (mL/ min)
During uncontrolled hemorrhage, bleeding intermittently
stops due to hypotension, vasoconstriction, or thrombus
rapid volume resuscitation. Instead, a central venous catheter should be placed for the infusion of vasopressors in
order to maintain an adequate perfusion pressure during
volume resuscitation if their use is anticipated.
formation.15 During controlled hemorrhage, hemodynam-
ics are normalized with uid resuscitation, whereas during
uncontrolled hemorrhage, permissive hypotension may be
allowed in order to minimize further blood loss.
15
Other classications for hemorrhage are based on loca-
MANAGEMENT OFPERIOPERATIVE BLEEDING
tion and vary depending on the nature of the injury and
the type of surgery. External hemorrhage involves open
fractures or amputations, and internal hemorrhage includes
Patients undergoing procedures at high risk for intraoperative blood loss (Table 12.4) or patients with known coagulopathies should undergo blood typing and cross- matching
prior to surgery. In cases where antibody screening is
positive, determining the availability of blood products
is imperative. In rare cases where multiple antibodies are
the thoracic, peritoneal, retroperitoneal, intramuscular, and
subcutaneousareas.
Antibrinolytics and exogenous clotting factors are
occasionally used both on- and o- label to prevent and
treat massive hemorrhage perioperatively. Several of these
agents are reviewed in Tables 12.6 and12.7.
detected, the anesthesiologist and surgeon should coordinate with the blood bank to ensure that a sucient number
of blood products are available based on the type of surgery.
MASSIVE TRANSFUSION PROTOCOLS
Intraoperative hemorrhage can be categorized as controlled or uncontrolled. During controlled hemorrhage,
bleeding is oen secondary to disruption of a major blood
Historically, massive transfusion has been dened as transfusion of greater than 10 units of blood within 24 hours or
TABLE12.6 ANTIFIBRINOLYTIC MEDICATIONS
Medication
Tranexamic
Acid
Aminocaproic
Acid
HYPOVOLEMICSHOCK 105
Indication Mechanism Dosing
Tooth extraction in patients with
hemophilia, cyclic heavy menstrual
bleeding (all other uses off- label)
Fibrinolytic bleeding Binds competitively to
Inhibits brinolysis by
displacing plasminogen from
brin, reduces plasmin activity
plasminogen, blocks binding
of plasminogen and plasmin
to brin, thus preventing
brinolysis
10 mg/ kg IV prior to surgery,
followed by same dose 3- 4
times/ day for 6- 8days
Initial 4- 5 g IV during rst
hour, then 1 g/ hr continuous
infusion (maximum 30 g/ day)
Special Considerations
Hypotension with rapid
IV injection, headache,
abdominal pain, back pain
Contraindicated in
disseminated intravascular
coagulation, rapid IV
injection can cause
hypotension, bradycardia
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