BACHELOR’S IN MEDICAL AND HEALTH SCIENCES

SEMESTER 4/2020

COURSE CODE
NBMH 2624

COURSE TITLE
TRAUMA AND EMERGENCY CARE

PREPARED BY:

Nama MOHAMAD ZUL AMREE HAMZAH

Matric Number 930108035557001
IC Number 930108035557
1.0 INTRODUCTION TO HYPOVOLEMIC SHOCK

The term “Hypovolemic shock” is defined as the rapid fluid loss or blood loss which results
in multiple organ dysfunction due to inadequate circulating body fluid, usually whole blood
or plasma. Porth (2015) states that Hypovolemic shock happened and caused blood loses
about 15% or more of intravascular circulating volume which is possibility to be in condition
of inadequate tissue perfusion and potential tissue necrosis. In this case, Hypovolemic shock
happened because of several factor including severe external haemorrhage or internal fluid
shifts as a result from dehydration (Garretson and Malberti, 2007). Besides, it is also can be
seen as a condition in which profound and widespread reduction of effective tissue perfusion
leads first to reversible, and then if prolonged, to irreversible cellular injury.

Life-threatening affected the blood pressure and one of the factors that lead to the
shock, a condition in which tissue perfusion is not capable of sustaining aerobic metabolism.
Shock can be produced by decreases in cardiac output (cardiogenic), by sepsis (distributive),
or by decreases in intravascular volume (hypovolemic). The latter may be caused by
dehydration from vomiting or diarrhea, by severe environmental fluid losses, or by rapid and
substantial loss of blood. A less common form of shock (cytopathic) may occur when the
mitochondria are incapable of producing the energy required to sustain cellular function.
Agents that interfere with oxidative phosphorylation, such as cyanide, carbon monoxide and
rotenone, can produce this type of shock. Haemorrhage is a medical emergency that is
frequently encountered by physicians in emergency rooms, operating rooms, and intensive
care units. Significant loss of intravascular volume may lead sequentially to hemodynamic
instability, decreased tissue perfusion, cellular hypoxia, organ damage, and death. This
review addresses the pathophysiology and treatment of hypovolemic shock produced by
haemorrhage, which is also known as haemorrhagic shock.

An intravascular volume depletion may occur with any condition which leads to
excessive extracellular fluid loss with or without loss of plasma protein. Hypovolemic shock
can occur secondary to haemorrhagic shock (rapid blood loss) which is rare but cause serious
complications and mostly occurs in obstetric situations. Basically, hypovolemic shock is
associated with disorders that cause an underlying hemodynamic defect of a low intravascular
volume and a reduction in myocardial contractility. It is a consequence of decreased preload
due to intravascular volume loss. The decreased preload diminishes stroke volume, resulting
in decreased cardiac output (CO). The systemic vascular resistance (SVR) is typically
increased to compensate for the diminished CO and maintain perfusion to vital organs. The
early stage of recognition and intervention will help to prevent death. Starling’s law of the
heart states that there is a direct relationship between the preload (the volume of blood within
the ventricle stretching the myocardium fibres) and contractility (the forcefulness of the
myocardial contraction). This will affect the stroke volume which is the volume of blood
ejected by the ventricle in one contraction and ultimately the cardiac output which is HR x
SV and equates to the amount of blood ejected in one minute (Aitken et al, 2015).

2.0 DISCUSSION ON THE SCIENTIFIC METHOD TO DETECT PATIENTS

WITH HYPOVOLEMIC SHOCK

In this part, there are several studies discussed about the scientific method in Hypovolemic
shock. Early recognition of hypovolaemic shock is vital for optimal care of the injured
patient. Whole blood loss from an open wound is an obvious cause for hypovolemic shock.
Acute blood loss or the redistribution of blood, plasma, or other body fluid predisposes the
injured patient to hypovolaemic shock. Absolute hypovolaemia refers to the actual loss of
volume that occurs in the presence of haemorrhage. Relative hypovolaemia refers to the
inappropriate redistribution of body fluids such as that that occurs following major burn
trauma. Acute blood loss is a very common problem following traumatic injury.

Rapid recognition and restoration of homeostasis is the cornerstone of the initial care
of any seriously injured patient. Delay in recognising and quickly treating a state of shock
results in a progression from compensated reversible shock to widespread multiple system
organ failure to death. Morbidity may be widespread and can include renal failure, brain
damage, gut ischaemia, hepatic failure, metabolic derangements, disseminated intravascular
coagulation (DIC), systemic inflammatory response syndrome (SIRS), cardiac failure, and
death. In response to a drop in BP, the sympathetic nervous system initiates a compensatory
response, aiming to maintain a enough CI.

Lending from Clarke and Ketchell (2011), baroreceptors in the aortic arch and carotid
sinus detect a decreased circulating volume and instigate a message to the cardiac vasomotor
centre, located in the medulla oblongata which is the stimulation of sympathetic nerves
initiates the release of catecholamines (epinephrine and norepinephrine) from the adrenal
glands, and resulting in vasoconstriction thus increased myocardial contractility. This
condition also supporting by Aitken et al, (2015) in which it is response attempts to maintain
organ perfusion by improving cardiac output. Therefore, BP= CO x SVR. If patient’s
tachycardic and signs of poor peripheral perfusion, which contributed to the development of
metabolic acidosis, reiterate the physiological process of hypovolaemic shock.

A study of blunt trauma found that a systolic blood pressure (SBP) <90mmHg will
only identify 61% of patients with active haemorrhage (sensitivity 61% and specificity 79%).
3.1% of patients with uncontrolled haemorrhage had undisturbed physiological variables.
Detecting hypovolaemic shock in the trauma patient with normal haemodynamic is reliant on
history, physical examination and pathology, including, base deficit, lactate, haematocrit and
haemoglobin. However, these tests are only of value when interpreted in a series. Initial
haemoglobin (Hb) of <=6g/l correlated well with mortality (48.4%) and vital signs. A low
level Hb (<8g/l) was found by Knottenbelt, in a review of 1000 trauma patients, to be an
indicator of serious ongoing haemorrhage. Lactate and base-deficit have also shown to
correlate well with vital signs and mortality. The ability and value of haemoglobin, lactate
and base-deficit, however, to predict blood loss in haemodynamically stable patients is
unknown. For the critically ill patient timely interpretation of appropriate investigations will
lead to essential treatment. Arterial blood gases (ABGs) offer useful information about gas
exchange, the metabolic status of the patient and the body’s ability to maintain a normal acid
base balance.

3.0 DISCUSSIONS ON THE CLINICAL FINDING SOURCES DETECTION OF

BLEEDING IN HYPOTENSIVE TRAUMA PATIENTS

Recognizing the degree of blood loss via vital sign and mental status abnormalities is
important. The American College of Surgeons Advanced Trauma Life Support (ATLS)
haemorrhagic shock classification links the amount of blood loss to expected physiologic
responses in a healthy 70 kg patient. As total circulating blood volume accounts for
approximately 7% of total body weight, this equals approximately five litres in the average
70 kg male patient. For the class 1 haemorrhagic shock, volume loss up to 15% of total blood
volume, approximately 750 mL. Heart rate is minimally elevated or normal. Typically, there
is no change in blood pressure, pulse pressure, or respiratory rate. For the class 1
haemorrhagic shock volume loss from 15% to 30% of total blood volume, from 750 mL to
1500 mL. Heart rate and respiratory rate become elevated (100 BPM to 120 BPM, 20 RR to
24 RR). Pulse pressure begins to narrow, but systolic blood pressure may be unchanged to
slightly decreased. For the class 1 haemorrhagic shock volume loss from 30% to 40% of total
blood volume, from 1500 mL to 2000 mL. A significant drop in blood pressure and changes
in mental status occur. Heart rate and respiratory rate are significantly elevated (more than
120 BPM). Urine output declines. Capillary refill is delayed. For the class 1 haemorrhagic
shock volume loss over 40% of total blood volume. Hypotension with narrow pulse pressure
(less than 25 mmHg). Tachycardia becomes more pronounced (more than 120 BPM), and
mental status becomes increasingly altered. Urine output is minimal or absent. Capillary refill
is delayed. Again, the above is outlined for a healthy 70 kg individual. Clinical factors must
be taken into account when assessing patients. For example, elderly patients taking beta
blockers can alter the patient's physiologic response to decreased blood volume by inhibiting
mechanism to increase heart rate. As another, patients with baseline hypertension may be
functionally hypotensive with a systolic blood pressure of 110 mmHg.

In a haemodynamically unstable trauma patient, there are five potential sites of major
blood loss: externally, long bones, the chest, the abdomen and the retroperitoneum. Blood
loss from fractures and lacerations can result in a significant amount of blood loss. The scalp
is a highly vascular region and may be associated with significant blood loss. It is, however,
extremely difficult to estimate the volume of bleeding from scalp and other lacerations due to
blood loss at the scene and end route to the hospital. External blood loss requires careful
visual inspection.

It is reported that a single long-bone fracture may result in 10-30% loss of total blood
volume. Bleeding from long bone fractures is present in approximately 40% of cases and is
usually evident from swelling due to haematoma formation. This is usually a contribution,
not a major ongoing cause of blood loss. Intrathoracic haemorrhage can be evaluated on a
chest x-ray, which should be performed as soon as possible within the patient’s arrival. There
are minor limitations to first mobile supine chest x-ray A small haemothorax can be initially
missed. However, a large haemothorax contributing to haemodynamic instability should not
be missed

The next part of the decision tree is crucial, trying to decide whether the blood loss is
in the abdomen or in the pelvic retroperitoneum or in both. At this point the AP pelvic
radiograph should be reviewed. If a pelvic fracture with possible disruption of the pelvic
ligaments causing an unstable fracture pattern is seen or suspected and there is probability of
pelvic arterial bleeding. The initial AP pelvic radiograph is the only guide to determine the
probability of pelvic bleeding. Disruptions involving only the pubic rami do not vertically or
rotationally unstabilise the pelvic ring, but when recognising a fracture of the pubic bone,
posterior disruption and probability of arterial bleeding must always be suspected. One must
also bear in mind that bilateral inferior/superior pubic ramus fractures (butterfly type fracture
from AP compression mechanism), acetabular fractures and even simple ramus fractures in
the elderly can lead to arterial bleeding causing hypotension.

The abdomen is the most difficult to assess in the rural and urban environment.
Diagnostic Peritoneal Aspiration (DPA) and Focused Abdominal Sonography in Trauma
(FAST) are the preferred diagnostic means to determine if there is intra-abdominal bleeding.
Although the availability of FAST is increasing, it is not available in all urban and rural
emergency departments. DPA is recommended if an EMST accredited clinician is available.
If neither FAST nor DPA can be undertaken, the clinician should examine the other four
sources for blood loss, upon exclusion of these it must be assumed that the patient has
intraabdominal bleeding until proven otherwise. In the face of continuing haemodynamic
instability and in the absence of external blood loss, long bone or pelvic fractures or any
evidence of bleeding on chest x-ray, immediate laparotomy is warranted.

4.0 DISCUSS ON THE ADVANCED MANAGEMENT OF THE MASSIVE

BLEEDING PATIENTS

The main goals of resuscitation are to stop the source of haemorrhage and to restore
circulating blood volume. Actively bleeding patients should have their intravascular fluid
replaced because tissue oxygenation will not be compromised, even at low haemoglobin
concentrations, as long as circulating volume is maintained. Haemoglobin concentration in an
actively bleeding individual has dubious diagnostic value because it takes time for the various
intravascular compartments to equilibrate. Rather, therapy should be guided by the rate of
bleeding and changes in hemodynamic parameters, such as blood pressure, heart rate, cardiac
output, central venous pressure, pulmonary artery wedge pressure, and mixed venous
saturation.

Treatment of hypovolaemic shock focuses on regaining adequate tissue perfusion via

restoration of fluid volume and BP. Consequently, fluid resuscitation will improve oxygen
delivery to cells, enabling aerobic respiration, which in-turn will help restore the acid-base
disparity (Garretson and Malberti, 2007). Guidelines proposed by the National Institute for
Health Care and Excellence (NICE) (2013) recommend a fluid challenge of a 500ml
crystalloid bolus, over 15 minutes for any patient suspected of hypovolaemia. Fluid
resuscitation using crystalloids provides a transient intravascular expansion and further
replaces accompanying fluid loss in interstitial and intracellular spaces. Hypertonic colloids
are normally only indicated to replace large volumes of fluid loss, or to restore low
haemoglobin levels, due to their higher cost and associated risks such as alteration in clotting
(Garretson and Malberti, 2007)

Sequential monitoring of vital signs and cardiac output are imperative when managing
a patient receiving a fluid challenge. Fluid boluses should be repeated until a rise of 3mmHg
or more is seen in the CVP, 5 to 10 minutes after the bolus has been fully administered
(Aitken et al, 2015). The CVP indicates the amount of blood returning to the heart and thus
cardiac output, therefore it is a useful guide when observing the effect of a fluid challenge
(Porth, 2015). However, CVP readings should not be used independently, as CVP can also be
sensitive to vasoconstriction. Vincent and Weil (2006) recommended using the CVP as a
safety guide to prevent hypervolemia, using quantitative clinical goals such as, blood
pressure, heart rate and MAP to help observe an increased peripheral perfusion.

For safe and effective administration of IV fluids NICE (2013) recommend using the
principles of the five R’s: Resuscitation, Routine maintenance, Replacement, Redistribution
and Reassessment. Treatment should focus on replacement of any electrolyte deficits
(Sherratt, 2014). Therefore, a maintenance plan including 500ml Hartmann’s solution and
500ml 5% dextrose was prescribed for Clive. The British consensus guidelines on
intravenous fluid therapy for adult surgical patients (Powell-Tuck et al. 2011) endorse
Hartmann’s solution over 0.9% saline as this can contribute to hyperchloremic acidosis,
particularly in the elderly. The isotonic nature of crystalloids such as Hartmann’s solution,
result in distribution within the interstitial space, ensuring adequate replacement of lost
electrolytes, such as potassium and sodium (Dougherty and Lamb, 2008).

To help distribute fluid evenly amongst the body’s compartments, the British National
Formulary (British Medical Association and Royal Pharmaceutical Society, 2016), advise for
an equal infusion of 500ml 5% dextrose, to aid intracellular hydration. The metabolism of
glucose, within dextrose, lowers the osmolarity of extracellular fluid creating a hypotonic
environment, causing a net movement of fluid into the cells moving down its pressure
gradient (Porth, 2015). Care though needs to be taken if there is any suggestion of altered
intracerebral pressure (ICP) as dextrose containing solutions can increase ICP. Management
priorities in the bleeding patient include controlling blood loss, replenishing intravascular
volume and sustaining tissue perfusion. When services are needed that exceed available
resources, it is of critical importance that early consultation with a trauma specialist and rapid
transportation to definitive care occurs.

After establishing a patent airway, ensuring adequate ventilatory exchange and

oxygenation and securing venous access, the highest priority in the bleeding patient is to
control haemorrhage. Because patient may bleed from multiple sites, it is imperative that the
attending medical officer establish strategies to address all sources of bleeding. Sources of
bleeding may be broadly classified as external or internal.

The Australian Resuscitation council advocates the use of direct pressure to gain
prompt control of external bleeding. The recommended method involves approximating the
wound edges if possible, holding an absorbent dressing firmly over the area with the heel of
the hand, and elevating the bleeding part. After bleeding is controlled the absorbent dressing
may be secured with a bandage. If bleeding continues through the initial dressing, apply a
second dressing over the first and secure with a bandage. Do not disturb the dressing once the
bleeding has been controlled. Arterial tourniquets are reserved for life-threatening bleeding
and when direct pressure to the wound has failed to stop the bleeding or when protruding
objects prevent direct pressure.

Evidence from numerous studies over the past two decades indicates that immediate
and definitive operative haemostasis is the optimal treatment for internal bleeding. To delay
leaves the patient susceptible to multi organ dysfunction and other complications. In the rural
and remote setting however, immediate operative haemostasis is limited by a lack of surgical
presence and or operating facilities at the site, and or lengthy transport times to institutions
capable of providing definitive operative haemostasis. Given these limitations the challenge
for the rural and remote physician is to rapidly identify patients who would benefit from early
transfer based on available local resources, manage any life-threatening injuries, and establish
prompt contact with the major referral centre, and the transport /retrieval service. Prolonged
time spent in a local emergency department poses a significant risk of mortality for the
internally bleeding patient.

Hypotensive resuscitation has been suggested for the hemorrhagic shock patient
without head trauma. The aim is to achieve a systolic blood pressure of 90 mmHg in order to
maintain tissue perfusion without inducing re-bleeding from recently clotted vessels.
Permissive hypotension is a means of restricting fluid administration until hemorrhage is
controlled while accepting a short period of suboptimal end-organ perfusion. Studies
regarding permissive hypotension have yielded conflicting results and must consider type of
injury (penetrating versus blunt), the likelihood of intracranial injury, the severity of the
injury, as well as proximity to a trauma centre and definitive haemorrhage control.

5 CONCLUSIONS

In conclusion, the people with milder degrees of shock tend to do better than those with more
severe shock. Even with immediate medical attention, severe hypovolemic shock may lead to
death. Older adults are more likely to have poor outcomes from shock. Mortality due to
hypovolemic shock is more variable. It depends on the cause and the duration until
recognition and treatment. Successful treatment of patients with shock requires prompt
recognition of the shock state and a thorough understanding of various types of shock to
reduce the mortality.

6 REFERENCE

rd
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Dougherty. L., & Lamb. J. (2008). Intravenous therapy in nursing practice. 2nd ed. Oxford:
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Garretson. S., & Malberti. S. (2007). Understanding hypovolaemic, cardiogenic and septic
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Knottenbelt. J.D. (1991). Low initial hemoglobin levels in trauma patients: an important
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