pbl 5

PBL 5

“A Bleeding Limb”

Part 1

A 30- year old woman from a road accident scene was brought to the Accident and Emergency Department. No active bleeding was observed in the injured lower limb nor elsewhere. On arrival, she was conscious, her pulse 80/min and blood pressure (B.P.) 100/80 mmHg. Half an hour later, she became restless, hands cold and clammy; pulse was 110/min and thready, and B.P. 80/70 mmHg

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keywords

30-yearold

woman

road accident

A/E dept

no bleeding

injured lower limb

conscious -> restlesss

80bpm -> 110bpm tachycardia

100/80 -> 80/70

thready pulse

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infers...

shock?

carviovascular? - no chest pain

hypovolemic - suggested, from the symptom

hypotention?

neurogenic shock

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we need to know...

whether there is a internal bleeding

urine output?

head trauma?

Glascow Coma Scale

pain.

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part 2

keywords

lacerating wound

controlled by first aider

limb bleeding remained controlled,

no swelling/distension

internal bleeding suspected

CVP

IV and blood.

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infers...?

maybe arterial leceration?

arterial damage due to crush injuries

what is compartment syndrome?

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hypothesis

her hypovolemia caused probably by an internal bleeding secondary to accident.

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learning issue

colloid/crystalloid - types of

compartment syndrome

extent at which we can lose blood

ligation

complication of hypovolemia

management!

physiological response to hypovolemia

major arteries and veins of lower limb

pathophysiology of hypovolemic shock

stages of shock

compensatory mechanism of shock

fluid management of shock patient / fluid resusitation

what is, how to measure, CVP

first aid measures at accident site

public health

medical ethics

mean arterial pressure vs pulse pressure

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colloid/crystalloid

crystalloid-based (Ringer's lactate, normal saline, D5W (dextrose 5% in water)

colloid-based (Voluven, Haemaccel, Gelofusin).

Whether crystalloids or colloids are best for resuscitation continues to be a matter for discussion and research.

Many fluids have been studied for use in resuscitation; these include

isotonic sodium chloride solution,

lactated Ringer solution,

2 hypertonic saline,

albumin,

purified protein fraction,

fresh frozen plasma,

hetastarch,

pentastarch,

dextran 70.

Proponents of colloid resuscitation argue that the increased oncotic pressure produced with these substances decreases pulmonary edema.

However, the pulmonary vasculature allows considerable flow of material, including proteins, between the intravascular space and interstitium.

Maintenance of the pulmonary hydrostatic pressure at less than 15 mm Hg appears to be a more important factor in preventing pulmonary edema.

Another argument is that less colloid is needed to increase the intravascular volume.

Studies have shown this to be true.

However, they still have not demonstrated any difference in outcome with colloids compared with crystalloids.

Synthetic colloid solutions, such as hetastarch, pentastarch, and dextran 70, have some advantages compared with natural colloids such as purified protein fraction, fresh frozen plasma, and albumin.

They have the same volume-expanding properties, but because of their structures and high molecular weights, they remain mostly in the intravascular space, reducing the occurrence of interstitial edema.

Although theoretic advantages exist, studies have failed to show a difference in ventilatory parameters, pulmonary function test results, days using a ventilator, total hospital days, or survival.

The combination of hypertonic saline and dextran also has been studied because of previous evidence that it may improve cardiac contractility and circulation.

Studies in the US and Japan have failed to show any difference when this combination was compared with isotonic sodium chloride solution or lactated Ringer solution.

Thus, despite the many available resuscitation fluids, current recommendations still advocate the use of normal saline or lactated Ringer solution.

In the US, one reason for the predominant use of crystalloids over the other resuscitative fluids is cost.

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compartment syndrome

Compartment syndrome (CS) is a limb-threatening and life-threatening condition observed when perfusion pressure falls below tissue pressure in a closed anatomic space. The current body of knowledge unequivocally reflects that untreated compartment syndrome leads to tissue necrosis, permanent functional impairment, and, if severe, renal failure and death.

Although long bone fractures are a common cause of compartment syndrome, other injuries are also a common antecedent to compartment syndrome. Approximately 50 years after vonVolkmann's seminal paper, Jepson described ischemic contractures in dog hind legs caused by limb hypertension after experimentally induced venous obstruction. In 1941, Bywaters and Beall reported on the significance of crush injury while working with victims of the London Blitz. These pioneers revealed mechanisms and consequences of compartment syndrome. In the 1970s, the importance of measuring intracompartmental pressures became apparent.

When fluid is introduced into a fixed volume, or when volume decreases with fixed volume, pressure rises.

Various osseofascial compartments have a relatively fixed volume; introduction of excess fluid or extraneous constriction increases pressure and decreases tissue perfusion, until no oxygen is available for cellular metabolism.

Elevated perfusion pressure is the physiologic response to rising intracompartmental pressure.

As intracompartmental pressure rises, autoregulatory mechanisms are overwhelmed and a cascade of injury develops.

Tissue perfusion is determined by measuring capillary perfusion pressure (CPP) minus the interstitial fluid pressure.

When this pressure falls below a critical threshold, injury results.

Normal cellular metabolism requires 5-7 mm Hg oxygen tension; this is easily maintained with the CPP averaging 25 mm Hg and interstitial pressure 4-6 mm Hg. However, rising interstitial pressure overwhelms perfusion pressure.

Matsen demonstrated that as intracompartmental pressure rises, venous pressure rises. When venous pressure is higher than CPP, capillaries collapse. The pressure at which this occurs is under debate; however, intracompartmental pressures greater than 30 mm Hg are generally agreed to require intervention.

At this point, blood flow through the capillaries stops. In the absence of flow, oxygen delivery stops.

Hypoxic injury causes cells to release vasoactive substances (eg, histamine, serotonin), which increase endothelial permeability. Capillaries allow continued fluid loss, which increases tissue pressure and advances injury.

Nerve conduction slows, tissue pH falls due to anaerobic metabolism, surrounding tissue suffers further damage, and muscle tissue suffers necrosis, releasing myoglobin. The end result is loss of the extremity and, possibly, the loss of life.

Anticoagulation therapy significantly increases the likelihood of compartment syndrome; remember to ask if patients are anticoagulated for any reason.

Certain physical signs are associated with compartment syndrome. After initial symptoms of pain or burning, decreased strength and eventually paralysis of the affected extremity occur. Follow-up physical examinations are important to determine if any progression of symptoms is noted.

http://emedicine.medscape.com/article/828456-overview

http://en.wikipedia.org/wiki/Fasciotomy

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how much blood we can lose where

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ligation procedure

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physiological responce to hypovolemic shock

a very nice visual summery of what would happen in the event of hypovol shock

pg 231 CAP 2003

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major arteries and veins of lower limb

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pathophysio of hypovolemic shock

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stages of shock

Classes of hemorrhage have been defined, based on the percentage of blood volume loss.

However, the distinction between these classes in the hypovolemic patient often is less apparent.

Treatment should be aggressive and directed more by response to therapy than by initial classification.

Class I hemorrhage (loss of 0-15%)

In the absence of complications,

only minimal tachycardia is seen.

Usually, no changes in BP,

pulse pressure,

or respiratory rate occur.

A delay in capillary refill of longer than 3 seconds corresponds to a volume loss of approximately 10%.

Class II hemorrhage (loss of 15-30%)

Clinical symptoms include

tachycardia (rate >100 beats per minute),

tachypnea,

decrease in pulse pressure,

cool clammy skin,

delayed capillary refill,

and slight anxiety.

The decrease in pulse pressure is a result of increased catecholamine levels,

which causes an increase in peripheral vascular resistance and a subsequent increase in the diastolic BP.

Class III hemorrhage (loss of 30-40%)

By this point,

patients usually have marked tachypnea and tachycardia,

decreased systolic BP,

oliguria,

and significant changes in mental status, such as confusion or agitation.

In patients without other injuries or fluid losses,

30-40% is the smallest amount of blood loss that consistently causes a decrease in systolic BP.

Most of these patients require blood transfusions,

but the decision to administer blood should be based on the initial response to fluids.

Class IV hemorrhage (loss of >40%)

Symptoms include the following:

marked tachycardia,

decreased systolic BP,

narrowed pulse pressure (or immeasurable diastolic pressure),

markedly decreased (or no) urinary output,

depressed mental status (or loss of consciousness),

and cold and pale skin.

This amount of hemorrhage is immediately life threatening.

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The human body responds to acute hemorrhage by activating the following major physiologic systems:

hematologic,

cardiovascular,

renal,

neuroendocrine

The hematologic system responds to an acute severe blood loss by activating the coagulation cascade and contracting the bleeding vessels (by means of local thromboxane A2 release).

In addition, platelets are activated (also by means of local thromboxane A2 release) and form an immature clot on the bleeding source.

The damaged vessel exposes collagen, which subsequently causes fibrin deposition and stabilization of the clot.

Approximately 24 hours are needed for complete clot fibrination and mature formation.

The cardiovascular system initially responds to hypovolemic shock by increasing the heart rate, increasing myocardial contractility, and constricting peripheral blood vessels. This response occurs secondary to an increased release of norepinephrine and decreased baseline vagal tone (regulated by the baroreceptors in the carotid arch, aortic arch, left atrium, and pulmonary vessels). The cardiovascular system also responds by redistributing blood to the brain, heart, and kidneys and away from skin, muscle, and GI tract.

The renal system responds to hemorrhagic shock by stimulating an increase in renin secretion from the juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin I, which subsequently is converted to angiotensin II by the lungs and liver. Angiotensin II has 2 main effects, both of which help to reverse hemorrhagic shock, vasoconstriction of arteriolar smooth muscle, and stimulation of aldosterone secretion by the adrenal cortex. Aldosterone is responsible for active sodium reabsorption and subsequent water conservation.

The neuroendocrine system responds to hemorrhagic shock by causing an increase in circulating antidiuretic hormone (ADH). ADH is released from the posterior pituitary gland in response to a decrease in BP (as detected by baroreceptors) and a decrease in the sodium concentration (as detected by osmoreceptors). ADH indirectly leads to an increased reabsorption of water and salt (NaCl) by the distal tubule, the collecting ducts, and the loop of Henle.

http://emedicine.medscape.com/article/760145-overview

http://emedicine.medscape.com/article/760145-treatment

hypovolemic shock - read it!

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fluid resusitation of shock patient

Two large-bore IV lines should be started.

The Poiseuille law states that flow is inversely related to the length of the IV catheter and directly related to its radius to the fourth power.

Thus, a short large-caliber IV catheter is ideal;

the caliber is much more significant than the length.

IV access may be obtained by means of

percutaneous access in the antecubital veins, cutdown of saphenous or arm veins,

or access in the central veins by using the Seldinger technique.

If central lines are obtained, a large-bore single-lumen catheter should be used. Intraosseous access has and continues to be used for hypotensive children younger than 6 years. Intraosseous access has also been used in hypotensive adults.1 The most important factor in determining the route of access is the practitioner's skill and experience.

Once IV access is obtained, initial fluid resuscitation is performed with an isotonic crystalloid, such as lactated Ringer solution or normal saline. An initial bolus of 1-2 L is given in an adult (20 mL/kg in a pediatric patient), and the patient's response is assessed.

If vital signs return to normal, the patient may be monitored to ensure stability, and blood should be sent for typed and cross-matched. If vital signs transiently improve, crystalloid infusion should continue and type-specific blood obtained. If little or no improvement is seen, crystalloid infusion should continue, and type O blood should be given (type O Rh-negative blood should be given to female patients of childbearing age to prevent sensitization and future complications

if a patient is moribund and markedly hypotensive (class IV shock), both crystalloid and type O blood should be started initially. These guidelines for crystalloid and blood infusion are not rules; therapy should be based on the condition of the patient.

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what is, how to measure, CVP

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first aid measures at accident site

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public health measures

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medical ethics

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mean arterial pressure vs pulse pressure

the blood pressure amplitude, also called pulse

pressure (PP), and is a function of the stroke

volume (SV) and arterial compliance (C =

dV/dP, !p. 188). When C decreases at a constant

SV, the systolic pressure Ps will rise more

sharply than the diastolic pressure Pd, i.e., the

PP will increase (common in the elderly; described

below). The same holds true when the

SV increases at a constant C.

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Shock index. The ratio of pulse rate (beats/min) to

systolic blood pressure (mmHg), or shock index, provides

a rough estimate of the extent of volume loss.

An index of up to 0.5 indicates normal or <10%>

up to 1.0 = <20–30%>

up to 1.5 = >30–50% blood loss and manifest shock

CAP2003 pg 230

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emergency procedure for suspected shock

ABC

Raise foot of bed

etcetc - look at OHCM

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pg 1926 of harrisons 17th

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"shock"

circulatory failure resulting in inadequate organ perfusion. gnenerally systolic BP <90mmhg.>

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signs-

pallor

increased pulse rate

decreased capilliary return (press nailbed)

air hunger

oliguria

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causes-

can be largely divided into;

pump failure

periphiral circulation failure

pump failure

cardiogenic shock

secondary - p.embolism, tension pneumothorax, cardiac tamponade

periphiral circulation failure

hypovolemia

anaphylaxis

sepsis

neurogenic

endocrine failure

iatrogenic