PROBLEM 2.

17 SG1
1. Discuss shock in terms of the:
a. different types
 Shock is a general term that refers to the depression or suppression of body functions
produced by any disorder. Circulatory shock refers to the shock developed by inadequate
blood flow throughout the body.
 Circulatory shock is primarily classified into four types:
i. Shock due to decreased blood volumehypovolemic shock
 It occurs when there is acute loss of at least 10% to 15% of blood. Loss of blood less than
10% may not produce any significant effect because of immediate compensatory
mechanism. Arterial and CO become 0 at about 40-45% blood loss
 Causes:
 Hemorrhage: Hemorrhagic shockacute hemorrhage
 Trauma: Traumatic shock
 Surgery: Surgical shock
 Burns: Burn shock
 Dehydration: Dehydration shock due to vomit, sweatfluid loss
ii. Shock due to cardiac diseasecardiogenic shock
 The heart itself is unable to efficient pump blood, thereby causing loss of perfusion
 Causes:
 Arrhythmia, particularly those which lead to reduced cardiac output
 Depressed activity of myocardium due to ischemiaMI
 Congestive cardiac diseaseVSD, ASD, PDA
 aortic valve/ mitral stenosis
iii. Shock due to obstruction of blood flowObstructive shock
 Physical obstruction of the heart or the great vessels. Shock developed due to the
obstruction of blood flow through circulatory system.
 Causes:
 Tension pneumothoraxphysical hole in chestinc in intrapleural becomes equal
to or greater than intrapulmonary pressurepush lung out of positionpress on heart
 Cardiac tamponadefluid accumulation around heart (serous fluid)compress the
heartdec vol of fillingharder to contract as well
 Pulmonary embolismblood cant return to left sidedec fluid in leftdec EDVdec
SVdec COdec BP
 Tumor in myocardium
iv. Shock due to increased vascular capacitydistribution shock
 The SVR decdilated vessels while others the CO is affected. In this case, the blood volume
is normal. Shock occurs because of inadequate blood supply to the tissues due to increased
vascular capacity. Capacity of the vascular system increases by the extensive dilatation of
blood vessels. It is also known as vasogenic or low resistance or distributive shock.

Types of Vasogenic
1. Sudden loss of vasomotor tone: Neurogenic shock
 Spinal cord injurysympathetic cut off to bottom body
 Hypoxic brain injuryaffect vasomotor centerloss of vasoconstriction
 Anesthesiageneral or spinal
2. Anaphylaxis: Anaphylactic shock
 Anaphylaxis means exaggerated allergic reaction to a foreign protein or antigen or any
other substance to which the person has been previously sensitized. Shock that develops
during anaphylactic reactions is called anaphylactic shock. Shock occurs because of
vasodilatation and sudden fall in blood pressure. It is caused by the chemical mediators
such as histamine, leukotrienes, IL that are secreted during anaphylactic reactionby
basophils and mast cells
3. Sepsis: Septic shock
 Sepsis is the pathological condition characterized by the presence of pathogenic organisms
or their toxins in blood or tissues. Shock developed during sepsis is known as septic shock or
blood poisoning.
 conditions when septic shock occurs
i. Infection of the uterus and fallopian tube, commonly occurring in abortion by
instrumentation
ii. Infection of peritoneum
iii. Spreading of skin infection due to bacteria like streptococci or staphylococci
iv. Spread of infection from any other part of the body.
4. Septic shock develops due to the depression of myocardium, dilatation of blood vessels and
increased permeability of capillary membrane. All these effects occur due to the toxic
substances released by bacteria. Septic shock is also called as vasogenic, cardiogenic or
hypovolemic shock.
Body also produced IL + TNFcause fever
5. Endotoxin shock Endotoxin shock is the shock developed by a bacterial toxin called
endotoxin. (lipopolysaccharide). It causes vasodilatation and depresses myocardial activity. It
also activates the macrophages to release cytokines. Endotoxin shock is very common during
the infection of alimentary tract by gram-negative bacteria like colon bacilli. It is actually
released from dead bacteria. Endotoxin shock can also occur in urinary tract infection.

b. signs and symptoms according to severity

 Each type of shock (cardiogenic, hypovolemic, neurogenic, anaphylactic, septic) involves
numerous clinical manifestations, signs, and symptoms that also may characterize other
conditions, making diagnosis difficult. If there are overlapping shock states that occur
simultaneously, the clear clinical manifestations confuse the diagnosis.
 An individual's history, risks, and situation are correlated with the specificity of the shock
state suspected or anticipated. For example, clinical manifestations common in septic shock
are fever, high heart rate, high respiratory rate, or elevations in immune responses, such as
increased levels of white blood cells.
  Elevated circulating blood glucose level, cyanosis, mottling, decreased urine output, and
decreases in blood pressure with altered mental status may be present in any shock state.
Subjective complaints often are nonspecific and general, such as chief complaints of
weakness, malaise, or shortness of breath.
 Following are the manifestations of circulatory shock:
I. Whenever cardiac output is decreased, arterial blood pressure drops down
II. Low blood pressure produces reflex tachycardia and reflex vasoconstriction
III. Tachycardia decreases the diastolic period. So, filling of the heart reduces leading to
decrease in stroke volume and systolic pressure. This decreases the pulse pressure below 20
mm Hg. Pulse also becomes feeble.
IV. Stagnant hypoxia develops because of decreased velocity of blood flow
V. Skin becomes pale and cold due to the vasoconstriction
VI. Along with hypoxia, cyanosis also develops in many parts of the body, particularly ear lobes
and fingertips, mucous membranes, lips
VII. Glomerular filtration rate (GFR) and urinary output are reduced due to fall in blood
pressure and constriction of renal blood vessels
VIII. Metabolic activities of myocardium are accelerated because of reduced blood flow and
increased heart rate. A large amount of lactic acid is produced, resulting in acidosis.
IX. Acidosis decreases myocardial efficiency and pumping action of the heart leading to further
reduction in cardiac output
X. So, the blood flow to vital organs is severely affected
XI. Lack of blood flow to brain tissues produces ischemia resulting in fainting and irreparable
damage of brain tissues
XII. Finally the damage of brain tissues and cardiac arrest kill the victim.
Specific shocks:
Cardiogenic
 Subjective complaints of chest pain, dyspnea, and faintness, along with feelings of
impending doom, are often revealed. Classic observable signs and symptoms of tachycardia,
tachypnea, hypotension, jugular venous distention, dysrhythmia, and low measured cardiac
output are hallmarks.
 Cyanosis; skin mottling; rapid, faint, or irregular pulses; low urine output; and occasional
peripheral edema are additional signs and symptoms of end-organ hypoperfusion.
 Myocardial dysfunction from fluid overload may result in extra heart sounds, pulmonary
edema (wheeze + crackles), hypoxemia, and elevated end-organ laboratory values.
 Metabolic abnormalities involving electrolyte imbalances, metabolic acidosis, and elevated
levels of inflammatory markers may result from or concur with the cardiac cascade of shock.
hypovolemic shock
 high SVR, pallor and cool extremities, increased thirst, oliguria, low systemic and pulmonary
preloads, and rapid heart rate.
neurogenic shock
 is a very low SVR, along with other indicators of excessive parasympathetic activity.
Bradycardia especially in the early stages. Bradycardia may cease when compensatory
mechanisms
 The ejection fraction remains high, indicating a healthy myocardium, whereas central
venous pressure decreases as the veins dilate. Neurogenic shock causes fainting if blood
pressure decreases to the point that cerebral metabolism is not sufficient to support
consciousness.
Anaphylactic shock
 Symptoms often affect multiple organ systems, including gastrointestinal (e.g., nausea,
abdominal pain, vomiting, diarrhea), cutaneous (e.g., erythema, pruritus, urticaria, or
angioedema), respiratory (e.g., shortness of breath, cough, rhinorrhea, tightening of throat,
difficulty swallowing, wheezing), cardiovascular (e.g., diaphoresis, pallor, hypotension), or
hematologic (e.g., fever, hemolysis). Other ominous clinical manifestations may be anxiety,
confusion, or impaired mentation. A precipitous decrease in blood pressure may account
for altered mental status and may result in oliguria.
Septic shock:
 Early symptoms
 fever usually higher than 101˚F (38˚C)
 low body temperature (hypothermia)
 fast heart rate
 rapid breathing, or more than 20 breaths per minute

 Severe sepsis is defined as sepsis with evidence of organ damage that usually affects the
kidneys, heart, lungs, or brain. Symptoms of severe sepsis include:
 noticeably lower amounts of urine
 acute confusion
 dizziness
 severe problems breathing
 bluish discoloration of the digits or lips
(cyanosis)

c. different stages
 Circulatory shock occurs in three stages:
1. First stage or compensated stage (non-
progressive)
 First stage is also called non-progressive
stage. When blood loss is less than 10% of
total volume, the blood pressure
decreases only moderately. And the regulatory mechanisms in the body operate
successfully to re-establish normal blood pressure and normal blood flow throughout the
body. Thus the shock becomes nonprogressive and the person recovers. Regulatory
mechanisms involve negative feedback control. Regulatory mechanisms are:
i. Baroreceptor mechanism
ii. Renal mechanism
iii. ADH mechanism.
2. Second stage or progressive stage
 Second stage is also called decompensated stage. When the shock is severe, positive
feedback system develops so that regulatory mechanisms become inadequate to
compensate. And the shock enters progressive stage. With immediate and appropriate
treatment, this stage of shock can be reversed. During this stage, blood pressure falls to a
low level, which is not adequate to maintain the blood flow to cardiac muscle. So the
myocardium starts deteriorating because of lack of nutrition and oxygen.
 Toxic substances released from tissues also suppress the myocardium. Particularly, the
bacterial toxin called endotoxin affects the myocardium severely. Loss of blood flow also
causes suppression of vasomotor system and the sympathetic system. This causes further
fall in blood pressure. Due to low pressure, thrombosis starts in small blood vessels like
capillaries. Now the capillary permeability increases allowing passage of fluid from blood
vessels into interstitial space. Finally because of tissue deterioration severe symptoms start
appearing. And the shock progresses to irreversible stage.
3. Third stage or irreversible stage.
 Third stage is the last stage prior to the collapse. It is also called refractory stage.
Irreversible stage leads to death regardless of type of treatment offered to the patient. It is
because the brain fails to function due to severe cerebral ischemia. The blood pressure falls
drastically. Even the infusion of blood fails to restore blood pressure. Finally, cardiac failure
occurs due to decrease in the myocardial activity and reduced arteriolar tone resulting in
death of the affected person. Details of this stage are given in Figure
d. consequences
cardiogenic shock hypovolemic
Neurogenic shock anaphylactic shock

Septic shock
 Mechanisms of Vasodilation in Shock.
 Vasodilatory shock is caused by the
inappropriate activation of vasodilatory
mechanisms and the failure of constrictor
mechanisms. Unregulated nitric oxide, by
regulating guanylate cyclase and generating
cyclic guanosine
monophosphate (cGMP), causes
dephosphorylation of myosin and, thus,
vasodilation. Nitric oxide synthesis and
metabolic acidosis activate the potassium
channels ( K ATP and K ca ) in the plasma
membrane of vascular smooth muscle.
 The resulting hyperpolarization of the
membrane presents the calcium that mediates
norepinephrine-induced and angiotensin II–
induced vasoconstriction from entering the cell.
Therefore hypotension and vasodilation stubbornly persist despite high plasma levels of
these hormones. In contrast, and unexpectedly, the plasma level of antidiuretic
hormone (ADH) (vasopressin) is low despite the presence of hypotension. The early,
massive release of ADH may result in future depletion
Obstructive shock

 CVP-central venous pressure (pressure in the thoracic vena cava near the right atrium)
 PCWP- pulmonary capillary wedge pressure

e. compensatory mechanisms
 The factors that cause a person to recover from moderate degrees of shock are all the
negative feedback control mechanisms of the circulation that attempt to return cardiac
output and arterial pressure back to normal levels. They include the following:
1. Baroreceptor reflexes
 Elicit powerful sympathetic stimulation of the circulation.
 Systemic vasoconstriction  increasing the total peripheral resistance.
 Veins and venous reservoirs constrict  ↑ venous return to the heart
 ↑heart rate as high as 160 to 180 beats/min.
2. Central nervous system ischemic response
 Elicits even more powerful sympathetic stimulation throughout the body but is not
activated significantly until the arterial pressure falls below 50 mm Hg.
3. Reverse stress-relaxation of the circulatory system
 Causes the blood vessels to contract around the diminished blood volume, so that the blood
volume that is available more adequately fills the circulation.
4. Activation of RAAS pathway
 Constricts the peripheral arteries and
reabsorbs sodium and water from the kidney
5. Formation of vasopressin (antidiuretic
hormone)
 Greatly increases water retention by insertion
of aquaporin 2 channels in principal cells
6. Compensatory mechanisms that return
the blood volume back toward normal
 Absorption of large quantities of fluid from the
intestinal tract,
 Absorption of fluid into the blood capillaries
from the interstitial spaces of the body
 increased thirst and increased appetite for salt
 Sympathetic reflexes maximally activated
within 30 seconds to a minute
 Angiotensin and vasopressin mechanisms
require 10 minutes to 1 hour to respond
 Readjustment of blood volume by
absorption require from 1 to 48 hours

f. events that leads to its irreversible state

 After shock has progressed to a certain
stage, transfusion or any other type of
therapy becomes incapable of saving the
person’s life. The person is then said to be
in the irreversible stage of shock.
 The cardiac output soon begins to fall
again, and subsequent transfusions have
less and less effect. By this time, multiple
deteriorative changes have occurred in the
muscle cells that over a long period,
depress heart pumping enough to cause
death.
 ↑↑ tissue damage, ↑↑ destructive
enzymes released, ↑↑acidosis
developed, and so many other
destructive factors are now in
progress.
 The high-energy phosphate reserves in
the tissues are greatly diminished
 all creatine phosphate has been
degraded
 all adenosine triphosphate  downgraded adenosine diphosphate adenosine
monophosphate  adenosine.
 Adenosine diffuses out of cells  uric acid  cannot re-enter cells to reconstitute
adenosine phosphate system.
 New adenosine can be synthesized at a rate of only about 2 per cent of the normal cellular
amount an hour
 Thus, one of the most devastating end results of deterioration in shock, and the one that is
perhaps most significant for development of the final state of irreversibility, is this cellular
depletion of these high energy compounds.

2. Discuss the management of hypovolaemic shock in terms of :

a. Types of intravenous fluids (IVF) used plus advantages,

Type Examples Advantages / Notes

- First-line fluids for hypovolemic shock (both

• Normal Saline (0.9% NaCl) hemorrhagic and non-hemorrhagic)
9g NaCl dissolved in 1 litres of water
25% remains in plasma and rest is .- Rapidly expand intravascular volume
lost to ECF
.- Inexpensive and widely available
Isotonic
crystalloids • Ringer’s Lactate (RL) / Hartmann’s
Solution .- RL is more physiologic (contains Na, Cl, K,
Ca, and lactate buffer)
Contains Na, K, Cl,Ca,and Na lactate
Most preferred in hemorrhagic shock
it minimizes acidosis due to .- Normal saline preferred if metabolic alkalosis
hyperchloremia is present, but large volumes can cause
hyperchloremic acidosis.

- More similar to plasma composition.

Balanced • Plasma-Lyte
crystalloids • Ringer’s Acetate - Reduced risk of metabolic acidosis.
- Lower chloride load → less renal injury.
 Type Examples Advantages / Disadvantages

- Maintain oncotic pressure longer than crystalloids

.- May be useful when large crystalloid volumes are
Natural causing edema
Albumin 5%, 25%
colloids
.- No clear survival benefit over crystalloids
.- Expensive.

- Provide rapid plasma expansion but increase risk of

renal injury, coagulopathy, and mortality.
Synthetic Hydroxyethyl starch (HES),
colloids Dextran, Gelatin
Not recommended in current guidelines.

Special Dextrose 5% in water - rapidly metabolized and remaining free water

solutions distributes rapidly evenly in fluid compartments
9g of dextrose per 100ml of
water
- 1liter = 670ml ICF + 330ml ICF + 70ml in blood
vessels
0.45 normal saline- hypotonic

- dextrose 5%= isotonic solution

Dextrose saline solution
- dextrose 10/20/30 %= hypertonic solution and
- isotonic solution of 4%
draws water from ICF to ECF > cerebral edema
dextrose/ 0.18% NaCI
- used to maintain fluid status
rather than resuscitation Used in hypoglycemia, dehydration, insulin shock
Not recommended in hypovolaemic shock
Half saline- 45% + 5% dextrose
used

Used in: diabetic ketoacidosis

and hypernatremia
 Type Examples Advantages / Disadvantages

 The primary treatment of haemorrhagic shock is to control the source of bleeding as soon
as possible and to replace fluid.
 In controlled haemorrhagic shock (CHS), where the source of bleeding has been
occluded, fluid replacement is aimed toward normalization of hemodynamic
parameters.
 In uncontrolled haemorrhagic shock (UCHS), in which the bleeding has temporarily
stopped because of hypotension, vasoconstriction, and clot formation, fluid treatment is
aimed at restoration of radial pulse or restoration of sensorium or obtaining a blood
pressure of 80 mm Hg by aliquots of 250 mL of lactated Ringer's solution (hypotensive
resuscitation).
 When evacuation time is shorter than 1 hour (usually urban trauma), immediate evacuation
to a surgical facility is indicated after airway and breathing (A, B) have been secured ("scoop
and run"). Precious time is not wasted by introducing an intravenous line.
 When expected evacuation time exceeds 1 hour, an intravenous line is introduced and fluid
treatment is started before evacuation. The resuscitation should occur before, or
concurrently with, any diagnostic studies.
IV Infusion
1. Crystalloid solutions
a.) 0.9 Normal Saline
 -contains 9 g of sodium chloride dissolved in 1000 mL of water
 -isotonic solution to ECF (290-300mOsm/L)
 -after distribution only 25% remain in plasma because most is lost to ECF
 -used in: hypovolemic shock, vomiting, diarrhoea, metabolic acidosis, metabolic alkalosis
 Precautionkidney + heart failrue
b.) Lactated Ringers (Hartmann’s solution)
 has a more physiological composition of sodium, potassium, chloride and calcium (NaCl, KCl,
CaCl2, sodium lactate)
 isotonic solution, same distribution as above
 -used in: severe burns, metabolic acidosis, acute blood loss, electrolyte imbalance
 Precautionliver disease + cerebral edema
c.) Dextrose 5% in water
 -contains 5 g of dextrose ( d -glucose) per 100 mL of water
 -This glucose is rapidly metabolised, and the remaining free water distributes rapidly and
evenly throughout the body’s fluid compartments i.e after 1L administration 670ml into ICF,
330 into ECF only 70ml in vessels
 -dextrose 5% is isotonic, while dextrose 10/20/30 % are hyper and irritate veinsthey are
hypertonixmove water from ICF to ECFused to treat cerebral edema, inc ICP
 -Used in: hypoglycemia, insulin shock, dehydration, cant eat due to injury, diluent for
medicine administration
 Precautionrenal/ cardiac compromise.
 Do not use in: inc intracerebral pressure or post op recovery
d.) 0.45 Normal Saline
 -hypotonic
 used in: diabetic ketoacidosis, hypernetrmia
 Precautionpulmonary edema, renal/cardiac compromise, not infused too quickly as it
leads to hemolysis.
 Contraindicationliver disease, burns, trauma
e.) plasma lyte-148
 -Plasma-Lyte 148 contains physiological concentrations of sodium, chloride and magnesium
but does not contain calcium or potassium.
 -isotonic

 Crystalloid is the first fluid of choice for resuscitation. Immediately administer 2 L of

isotonic sodium chloride solution or lactated Ringer’s solution in response to shock from
blood loss. Fluid administration should continue until the patient's hemodynamic become
stabilized. Because crystalloids quickly leak from the vascular space, each litter of fluid
expands the blood volume by 20-30%; therefore, 3 L of fluid need to be administered to
raise the intravascular volume by 1 L.
• Classified according to tonicity

2. Colloidscontain large particles that exert an oncotic pressure and may occur naturally
(e.g., albumin) or be synthetically modified (e.g., gelatins, hydroxyethyl starches, dextrans).
colloid remains largely within the intravascular space until the colloid particles are removed by
the reticuloendothelial systemhalf life of 6-24hrs
 inc risk of coagulopathy, more expensive, reticuloendothelial system dysfunction, pruritus
and anaphylactic reactions.
 Alternatively, colloids restore volume in a 1:1 ratio. Currently available colloids include
human albumin, hydroxy-ethyl starch products (mixed in either 0.9% isotonic sodium
chloride solution or lactated Ringer’s solution), or hypertonic saline-dextran combinations.
The sole product that is avoided routinely in large-volume (>1500 mL/d) restoration is the
hydroxy-ethyl starch product mixed in 0.9% isotonic sodium chloride solution because it has
been associated with the induction of coagulopathy. The other products have not been so
implicated.

3. dextrose saline solutions

 -The isotonic solution of 4% dextrose/0.18% sodium chloride is widely used as a solution for
maintenance of fluid status when replacement of losses rather than resuscitation
 appropriate replacement of sodium, chloride and glucose when used as a single fluid at 80–
100 mL/h for an average-sized adult.
 -reduce risk of excessive NaCl replacement.
 -half normal saline 45% + 5% dextrose normally used. But commercially available is
5%dextrose with .9% saline in 500ml
 In patients with haemorrhagic shock, hypertonic saline has the theoretical benefit of
increasing intravascular volume with only small amounts of fluid. The combination of
dextran and hypertonic saline may be beneficial in situations where infusion of large
volumes of fluid may be harmful, such as in elderly persons with impaired cardiac activity.
Additional trials will be required before this combination is accepted as standard of care.
extra:
Indication for IV:
 BP is within normal and not inclining ( not >140)
 RR- within normal (12-20)
 HR or pulse - within normal (60 - 100)
 anxious, alert, responsive
 urine output rate at 30ml/30min

 Sympathomimetic drugs best in neurogenic and anaphylactic shock but not in hemorrhagic
 Glucocorticoids in last stage of shock, why?
 they inc strength of heart in late stage
 stabilize lysosomal enzymes in late stage
 might aid in metabolism of glucose by the severely damaged cells

b. Indications for use of blood in hemorrhagic shock

 shock by hemorrhagewhole blood transfusion (plasma + platelets)
 shock by plasma loss give plasma
 shock by dehydrationIV fluids
 if blood not availablecan give plasma as body can survive with half the normal hematocrit
 if plasma not availableuse plasma substitutes like Dextran solution (effectively keep fluid
in vessels)

Indication for blood:

• Continuously declining BP
• Continuously elevated
 RR : >20 or >30 breaths/min
 HR or pulse: > 100 or 140 beats/min
• anxious, confused, lack or alertness or unconsciousness
• Dec urine output over time
• Cyanosis and cool peripheries
Note: the greater the blood loss the more the requirement for Blood transfusion
• Calculate Blood transfusion volume according to weight and age.
• 1 kg = 90ml of blood

Blood Use  Packed RBCs

 PRBCs should be transfused if the patient remains unstable after 2000 mL of crystalloid
resuscitation. For acute situations, O-negative non crossmatched blood should be
 administered. Administer 2 U rapidly, and note the response. For patients with active
bleeding, several units of blood may be necessary.
 There are recognized risks associated with the transfusion of large quantities of PRBCs. As a
result, other modalities are being investigated. One such modality is haemoglobin-based
oxygen carriers (HBOC). Clinical application has been limited by its toxic effect profile.
However, research is ongoing on the use of these products.
 If at all possible, blood and crystalloid infusions should be delivered through a fluid warmer.
A blood sample for type and cross should be drawn, preferably before blood transfusions
are begun. Start type-specific blood when available.
 Patients who require large amounts of transfusion inevitably will become coagulopathic.
Fresh frozen plasma generally is infused when the patient shows signs of coagulopathy,
usually after 6-8 U of PRBCs. Platelets become depleted with large blood transfusions.
Platelet transfusion is also recommended when a coagulopathy develops.
 Special concern
 One situation that may arise is the transfusing of massive amounts of blood products into a
Jehovah's Witness. This error occurs on occasion. Despite acting in the patient's best
interest (prior to knowing that the patient would not want a blood transfusion), this error is
a major incident for the patient. In this situation, honesty with the patient and the family
member(s) is the rule. Involve the hospital's risk manager early. Family conferencing with a
clergy member sometimes is helpful as well.

PROBLEM 2.17 SG2

1. Discuss the management of a trauma patients in terms of:
Resuscitation is a dynamic and intense period of medical care guided by the initial and
continuous assessment of the patient. It combines diagnostic and therapeutic manoeuvres to
rapidly identify and treat life-threatening
disorders in order of clinical priority
a. pre-hospital care
 Prehospital care of trauma patients is
situation-dependent and centered
on stabilization of the patient and
prompt transport to a hospital.
 Nonmedical personnel trained in
basic life support may provide life-
saving interventions
 Initial assessment: Follow the A,B, C stabilise the cervical spine and assess the level of
consciousness.
 Levels of consciousness:
● A- alert
● V- respond to verbal stimuli
● P- responds to pain
● U- unresponsive

How to determine which patient to transport 1st?

 dangerous mechanism of injury, history reveals loss of consciousness and difficulty
breathing, abnormal initial assessment and poor general impression.
Which type of exam?
 dangerous, generalised mechanism or altered mental status= rapid trauma survey
 dangerous focused mechanism, suggesting isolated injury and no significant life threat=
focus exam
trauma survey:
 Brief assessment of the head, neck, chest, abdomen, pelvis and extremities to identify
immediate life threats.
● Baseline vital signs
● SAMPLE history S-symptoms, A-allergies, M-medication, P-PMHX, L-last oral intake, E- events
prior to accident
● If altered level of consciousness do brief neurological exam. If altered LOC, do a brief
neurological exam to rule out increased intracranial pressure (pupils, GCS, cushing reflex
 -check the patient’s back -transfer the patient to the backboard

What interventions?
 Low-threshold interventions that may be performed by emergency personnel prior to
transport to a hospital include, but are not limited to:
 Placement of a cervical collar (if cervical spine trauma is suspected based on primary
survey or mechanism of injury)
 Intubation or oxygen delivery via nasal cannula; (if respiratory distress or altered mental
status is suspected)
 Administration of intravenous fluid; (if hemorrhage or hypotension is suspected)
 Administration of analgesia
 Placement of tourniquets or pressure bandages for control of bleeding
 CPR

 Special conditionLoad and go situation: immediate transfer of patient from scene

 Whensignificant mechanism of injury or poor general impression, initial assessment
reveals altered mental status, abnormal airway or respiration, abnormal circulation (shock
or uncontrolled breathing)
 Signs of impeding shock
 Abnormal chest exam ● Tender, distended abdomen ● Unstable pelvis ● Bilateral femur
fractures

b. preparation in emergency department

 prepare personnel
 4 discussion points:
i. What do we know? The stem that you receive from the EMS call
 ii. Run through the most likely immediate life threatening issues/ injuries
iii. Discuss contingencies if those actions fail
iv. Assign logistical tasks to team members.
 Mental preparationincluding visualization of complex tasks, deep breathing exercises,
and positive self-talk to help focus.
 Consider calling for help early (anesthesia, surgery, orthopaedics, paediatrics etc) if you
work in a center that does not have a dedicated trauma team. Tie up loose ends with other
patients in your ED if time permits before the trauma patient arrives, so that after you’re
done managing the trauma patient, your ED is not a disaster zone

Equipment preparation
 Ensure that the ED has a well thought out trauma cart that will contain the gear that you
may require:
 thoracostomy kit minimally invasive procedure in which a doctor inserts a thin plastic

tube into the pleural space

 -pelvic binder device used to compress the pelvis in people with a pelvic fracture in an
effort to stop bleeding.
 -cricothyrotomy kit placing a tube through an incision in the cricothyroid membrane
(CTM) to establish an airway for oxygenation and ventilation

 crash cart is a set of trays/drawers/shelves on wheels used in hospitals for transportation

and dispensing of emergency medication/equipment at site of medical/surgical emergency
for life support protocols (ACLS/ALS)
 contents may include but are not limited to:
 Monitor/defibrillators, suction devices, and bag valve masks (BVMs) of different sizes
 Advanced cardiac life support (ACLS) drugs such as epinephrine, atropine, amiodarone,
lidocaine, sodium bicarbonate, dopamine, and vasopressin
 First line drugs for treatment of common problems such as: adenosine, dextrose,
epinephrine for IM use, naloxone, nitroglycerin, and others
 Drugs for rapid sequence intubation: succinylcholine or another paralytic, and a sedative
such as etomidate, propofol or midazolam; endotracheal tubes and other intubating
equipment
 Drugs for peripheral and central venous access
 Pediatric equipment (common pediatric drugs, intubation equipment, etc.)
 Other drugs and equipment as chosen by the facility
c. primary survey (ATLS)
 The management of trauma patients begins with the primary survey (also commonly
referred to as Advanced Trauma Life Support, or ATLS). The primary survey consists of 5
steps (ABCDE approach) that are performed in order.

1Airway assessment (and cervical spine stabilization)

 If appropriately answering questions, patient has a patent airway (at least for the moment)
 Observe patient for signs of respiratory distress (tachypnea & stridor)
 Inspect mouth and larynx for injury or obstruction (e.g., blood, vomit, burns, soot)
 Assume cervical spine injury in blunt trauma patients until proven otherwise
 If patient is unconscious (and therefore unable to protect their airway) or in respiratory
distress, the threshold for intubation is very low.
 Patients may be intubated or ventilated with the anterior portion of the cervical collar
removed, or with their neck manually stabilized.
 If orotracheal intubation is difficult, perform a cricothyrotomy.

2Breathing
 Assess oxygenation status with pulse oximetry.
 Inspect and auscultate chest wall for injuries (e.g., absent breath sounds, asymmetric or
paradoxical movement)
 In unstable patients, do not delay treatment of tension pneumothorax or hemothorax in
favor of imaging.

3Circulation (and hemorrhage control)

 Assess circulatory status by palpation of central (e.g., carotid, femoral) and peripheral (e.g.,
radial, popliteal, posterior tibial, dorsalis pedis) pulses
 Blood pressure should be measured if it can be done expediently, but it can be skipped
if it would delay the rest of the primary survey.
 Place two large-bore intravenous lines (at least 16 gauge) for blood typing and crossmatch,
and resuscitation (if needed).
 If intravenous line placement is not possible or difficult, intraosseus line should be used
instead.
 Control on-going hemorrhage with manual pressure or tourniquets.
 Emergency thoracotomy; may be performed in patients with recent loss of pulses
(especially in patients with stab wounds to the chest).
 If patient is hypotensive, administer a bolus of intravenous saline.
 If history of hemorrhage or on-going hemorrhage, transfuse type O blood.
 If significant hemorrhage and persistent hemodynamic instability, transfuse plasma,
platelets and red blood cells at 1:1:1 ratio.
 Focused Assessment with Sonography for Trauma (FAST) exam; is usually performed,
especially for hemodynamically unstable patients
 May be performed during secondary survey in hemodynamically stable patients
 Remember hypovolemic shock due to hemorrhage requires loss of ∼ 1.5 L of blood. Keep in
 Some patients may require emergent reversal of anticoagulation

mind the compartments where large amounts of blood may go:

 Outside (external hemorrhage)
 Thoracic cavity
 Pelvic cavity
 Abdominal cavity
 Thighs (e.g., multiple femur fractures)
 See Shock LC

4Disability (and neurological evaluation)

 Assess patient's Glasgow Coma Scale score
 See Glasgow Coma Scale (GCS)
 A GCS score ≤ 8 is an indication for intubation
 Assess pupillary size
 If patient is interactive, assess motor function and light touch sensation.

5Exposure (and environmental control)

 Undress patient completely.
 Examine body for signs of occult injury, including patient's back.
 If patient is hypothermic, cover with warm blankets and warm intravenous fluids.
 Palpate for vertebral tenderness and rectal tone.

d. secondary survey
 Performed after the primary survey has been completed and patient is deemed stable
 Complete history and thorough physical examination
 Head-to-toe examination
 including spine and digital rectal exam
 Take care to inspect the ‘hidden zones’ such as axillae, perineum and natal
cleft.
 Additional diagnostic tests are tailored to remaining symptoms, mechanism of injury, and
patient comorbidities.
AMPLE history
 Allergies
 Medications currently taking
 Past medical history
 Last ate/drank
 Events related to injury.
Imaging
 determined by physiology, mechanism and anatomy of injury and the clinical
question.
 Plain x-rays and ultrasound have role in immediate assessment of the injured patient
 Full-body CT is the gold standard of trauma imaging
 Main goal is to minimize the risk of missed injuries.

e. tertiary survey

 Delayed re-examination of the patient (usually ∼ 24 hours after admission)

 The primary and secondary surveys are repeated within 24 hours to identify evolving or
previously missed injuries.
 A ‘problem list’ is then created for each injury with a coherent management plan and
the details of involved specialties
 Main goal is to detect changes due to previously undetected injuries.

2. Discuss pneumothorax in terms of:

Pneumothorax refers to air in the pleural cavity. The presence of air at atmospheric pressure in
the pleural cavity and the separation of the pleural membranes by air prevent expansion of the
lung, leading to atelectasis (lung collapse). When pneumothorax is caused by a malignant
tumour or trauma, fluid or blood may also be present in the cavity. For example, with fluid in
the more dependent area and air above it, the condition could be called hydropneumothorax.
Chest x-rays can determine the type and extent of pneumothorax.
a. types and their causes
[Link] pneumothorax occurs when air can enter the pleural cavity through an opening
directly from the internal airways. There is no opening in the chest wall. This can be a simple or
spontaneous pneumothorax or can be secondary to another disease.

ASimple or spontaneous pneumothorax occurs when a tear on the surface of the lung allows
air to escape from inside the lung through a bronchus and the visceral pleura into the pleural
cavity. As the lung tissue collapses, it seals off the leak. The apex of the upright lung is subject
to greater mechanical stress than the base because the weight of the lung pulls down on
itmost prone.
 Simple pneumothorax often occurs in young men who have no prior lung disease but
perhaps an idiopathic bleb or defect on the lung surface. Following collapse, the
mediastinum can shift toward the affected lung, allowing the other lung to expand more.
Causethin + tall, preg, smoking inc risk

B Secondary spontaneous pneumothorax A pneumothorax secondary to diseased lungs

causes more severe symptoms and takes longer to heal. Rare precipitating factors are coughing
fits, sneezing, breath-holding, loud music, playing a wind instrument and thunderstorm. Causes:
 form of COPD, including emphysema and chronic bronchitis
 acute or chronic infection, like tuberculosis or pneumonia
 lung cancer
 cystic fibrosis
 asthma
 severe acute respiratory distress syndrome (ARDS)
  -idiopathic pulmonary fibrosis
 collagen vascular disease

[Link] open pneumothorax, air enters the pleural cavity through the opening in the chest wall
and parietal pleura, causing immediate atelectasis on the affected side. Because more air
enters the pleural cavity during inspiration, the mediastinum pushes against the unaffected
lung, limiting its expansion. Subsequently, on expiration, as air is pushed out of the pleural
cavity through the opening, the mediastinal contents shift back toward the affected side.
 Cause puncture from a fractured rib, inaccurate insertion of a cannula, high-volume
mechanical ventilation, rupture of an emphysematous bulla or drug abuse with prolonged
Valsalva breath-holds
 These abnormal movements occur as the pressure changes with rib movements on
inspiration and expiration. This mediastinal flutter or “to-and-fro” motion impairs both
ventilation in the unaffected lung and venous return through the inferior vena cava.

[Link] pneumothorax is the most serious form of pneumothorax.

 This situation may result from an opening through the chest wall and parietal pleura (open
pneumothorax) or from a tear in the lung tissue and visceral pleura (closed pneumothorax)
that causes atelectasis. The pattern of damage creates a flap of tissue or a one-way
valve effect, whereby the opening enlarges on inspiration, promoting airflow into the
pleural cavity.
 However, on expiration, the opening is sealed off, preventing removal of air from the
pleural cavity. Thus, with each inspiration this lesion leads to continual increases in the
amount of air in the pleural cavity. Pressure increases on the affected side eventually push
the mediastinal contents against the other lung, compressing the other lung and the
inferior vena cava. Severe hypoxia and respiratory distress develop quickly and can become
life threatening if the source of the valve effect and increasing intrapleural pressure is not
treated.
 Cause a blow to the chest, a penetrating injury, changes in pressure when diving, flying,
or mountaineering, a spontaneous pneumothorax progressing to a tension type, some
medical procedures
 b. mechanism of development

c. pathophysiological effects and clinical features

Signs and Symptoms
 The general signs of pneumothorax include the following:
 Atelectasis
 Dyspnoea
 Cough
 Chest pain
 Breath sounds are reduced over the atelectatic area
 Unequal chest expansion and mediastinal shift vary with the type of pneumothorax
 Hypoxia develops and leads to a sympathetic response, including anxiety, tachycardia,
and pallor
 Interference with venous return leads to hypotension
Closed Open Tension

Cause Spontaneous, Puncture wound through chest Open—puncture through thorax

idiopathic wall Closed—tear in lung surface
Ruptured Both with flap or one-way valve
emphysematous bleb
Air entry From inside lung From outside body through Through the thorax or tear in lung
 through tear in opening in thorax and parietal surface
visceral pleura pleura
Effects Atelectasis Atelectasis Atelectasis
Leak seals as lung Air enters pleural cavity with Air enters pleural cavity with each
collapses each inspiration and leaves inspiration
with each expiration Flap closes with expiration, and air
pressure increases in pleural cavity
pressure
One lung impaired Unaffected lung compressed Unaffected lung increasingly compressed
by mediastinal shift on by mediastinal shift
inspiration
No additional Mediastinal flutter impairs Mediastinal shift reduces venous return
cardiovascular effects venous return to heart to heart
Signs All three types: Increased, labored respirations with dyspnea, tachycardia, pleural pain, and
asymmetric chest movements
Breath sounds absent “Sucking” noise if large Breath sounds absent on affected side
Tracheal swing Tracheal deviation to unaffected side
Decreased blood pressure Increasing respiratory distress
Shock, distended neck veins, cyanosis
Hypoxemia Moderate hypoxemia Severe hypoxemia

d. management of small, medium and large pneumothoraces

Emergency Treatment for Pneumothorax
I. Transport to a hospital as soon as possible.
II. An open pneumothorax or sucking wound is covered with an occlusive dressing or covering
to prevent the air moving in and out of the pleural cavity. The dressing should be checked to
ensure that a tension pneumothorax has not developed.
III. Penetrating objects should not be removed from the chest wall until medical assistance is
available.
IV. If possible, tension pneumothorax should be converted to an open pneumothorax by
removing loose tissue or enlarging the opening.

Initial Management
 When tension pneumothorax is suspected or the patient has severe respiratory distress,
emergent needle decompression or tube thoracostomy should be performed. Needle
decompression can be done at the bedside using a large-bore Angio catheter needle. The
needle is introduced in the second intercostal space midclavicular line. The needle is
retracted and the catheter is left in place and attached to a three-way stopcock and a three-
chamber system connected to suction. Alternative sites for needle decompression include
the fourth or fifth intercostal space in the anterior axillary line.
 100% oxygen administration reduces the partial pressure of nitrogen in pleural capillaries,
consequently 4x the rate of pneumothorax absorption, and should be administered to all
patients with pneumothorax.
 When the patient is hemodynamically stable and tension pneumothorax is not suspected,
further treatment is based on the size of the pneumothorax and the presence or absence of
associated symptoms.
 If the pneumothorax is small (<2 cm between lung and chest wall on CXR) and the patient is
asymptomatic, the patient can be treated with observation alone. Repeat imaging should be
performed to ensure stability/resorption of the pneumothorax. Some studies have shown
that using a cutoff of 35 mm for deciding which patients can be managed with observation
is reasonable in selected patients with non-occult traumatic pneumothoraxes after
consultation with trauma consultants.
 If the pneumothorax is large (>2 cm), or if the patient is symptomatic with chest pain and
dyspnea, initial management should focus on removing air from the pleural space.
 Needle aspiration is the treatment of choice in the clinically stable patient with a large
primary spontaneous pneumothorax. Needle aspiration can be done at the bedside using a
large-bore Angio catheter needle or a commercially available catheter aspiration kit. The
needle is introduced in the second intercostal space midclavicular line. The needle is
retracted and the catheter is left in place and attached to a three-way stopcock and a large
syringe. Air is aspirated until resistance is met or the patient experiences significant
coughing. Repeat CXR is done immediately after aspiration and again in 4 to 24 hours to
document re-expansion of the lung.
 If there is improvement but not complete resolution of pneumothorax after the aspiration,
the catheter can be attached to a Heimlich (one-way) valve or to water seal to allow further
lung expansion. Some stable patients can be discharged home with a Heimlich valve in place
if close follow-up monitoring can be obtained.
 Tube thoracostomy is the treatment of choice for patients with a large secondary
spontaneous pneumothorax or in patients with large primary spontaneous pneumothorax
that did not resolve with needle aspiration. Tube thoracostomy can be performed at the
bedside preferably using the Seldinger technique with a small to medium bore chest tube
(<14 Fr). The chest tube should be inserted in the second intercostal space in the
midclavicular line. Alternate sites for tube thoracostomy include the fourth or fifth
intercostal space in the anterior axillary line.