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Hemorrhage is classified according to:
Source
Time of onset
Site of bleeding -> either internal or external bleeding.
Hemorrhage according to the source of-1
bleeding:
1- Arterial Hemorrhage:
Ex. A patient with RTA road traffic accident, trauma (gun shotto his lower limb) so there's arterial hemorrhage. It is a brightfresh blood (Oxygenated blood) and its pulsatile (in systoleit gives ejection, and stops in diastole) so it works as on/offpulsatite. So in an operation there's a bleeding if itspulsatile bleeding we know this is an arterial hemorrhagefor an injured artery.
2- Venous Bleeding:As we know that the pressure is lower in the veincompared to the artery, so the injured vein is notpulsatile but its continuous . Always we have venousreturn to the heart so this give the venous bleeding thecontinuity with a steady and copious flow, now if you look atthe surgical field you'll find it's full of blood, but you can't find
the source; one of the veins is injured with a steady slowcontinuous flow of the blood.About the color of blood its dark red (Deoxygenated blood).
3- Capillary Bleeding:Usually it's like the arterial bleeding; bright red blood oftenrapid ooze not pulsatile.
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2- Onset of the Bleeding:
primary hemorrhage: A bleeding developed at the time ofinjury or during surgery (intra-operative), usually it's the easiest to
handle; because we know the source of it. Ex. In an operation ofGastrictomy and during this surgery the operator injured an artery.OR someone injured with a shot and he had a bleeding artery sothese are examples for primary hemorrhage.
Reactionary hemorrhage: Follow the primary hemorrhagewithin 24 hrs and most commonly in the first 4-6 hrs after theprimary hemorrhage (Mainly due to slipping of a ligature,dislodgment of a clot or cessation of reflex vasospasm.
Ex. A. splenctomy operation for hypotensive patientin shockandduring this operation and after excision for hilum of spleen forsplenic artery after the operation he received IV fluids and bloodand this led to increase the pressure and venous return so this ledto escaping the surgical sutures due to the high pressure so thiswhat we called reactionary hemorrhage (slipping of a ligature).
B. patient in ER with a shock and internal hemorrhage he had aclot at injury site and this clot closed the source of bleeding thenhe given blood and fluids so this 'll increase the pressure and bythat the clot will be dislodged and the bleeding continue again(Dislodgment) .
C. After the arterial injury will be vasospasm of the artery (it maycontinued to 4-5 hrs then the reflex mechanism removed and thereactionary hemorrhage takes place).
Secondary hemorrhage: usually occurs one week to twoweeks after primary injury.
Ex. Patient with a drain in his abdomen after the surgery and led tonecrotic pressure on one of the arteries then the artery opened.
Or infection in the operation place which made it a fragile. Orpatient with cancer and after operation the cancer eroded theartery again and causing secondary hemorrhage.
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3-Site of the hemorrhage:
visible & is called revealedisItExternal hemorrhage:hemorrhage.
, liver, kidney,Ruptured spleenEx.Internal hemorrhage:ruptured ectopic gestation or pt' with closed fracture (fractured
femur but the skin and fascia intact).
Sometimes the internal bleeding could converts to external
one Pt' with gastric cancer and erosion for one of the gastric
arteries so this is internal bleeding but after that he vomited blood
(Hematemesis) then defecated blood (Melena).
Pt' with gunshot and blood loss and the doctor should estimate
the loosed blood ,, how this occurs?
kg\85ml-80ximately hasAccording to age the infant appro
assume that you've a newborn and his weight is 4kg
(4kg*80=320ml) so Total blood volume ~300 ml, if he loses100ml so this equal 1/3 blood so this considered a big problem for
a newborn.
For Adult 65-75ml/kg ~70 ml/kg and his weight is 70 kg so
(70*70=4900) so Total blood volume ~5000ml (5 liters ) so if this
Pt' loses 100ml thats mean 100/5000 (1/50) of his blood and this
is very small ratio for an adult. And thats mean the infants can't
tolerate blood loss like adults and if we give them fluids the amount
should be small not the same as adults.
We have multiple measures to measure the amount of
bleeding:
1.Blood clot the size of fist is roughly equal to 500ml so each
clot = 0.5 liter and this is useful way in operations.
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2.Swelling in closed fracturesThe estimated blood loss in
closed fractured femur approximately equal ( 0.5-2 L) for tibia it'll
be less than that (0.5-1.5 L) .
3. On the operation room Swab weighing, blood loss can bemeasured by weighing swabs after use & subtracting the dryweight. (1gm BLOOD =1ml) in short operations
For long operations (thoracoabdominal surgeries or abdomino-
perineal operations) >4 hrs so (1gm BLOOD =2ml)
Ex. 200gm of blood in gauzes = 2*200 =400 ml blood loss.
4. Measuring the blood collected in the suction & drainage
bottles
5. Hemoglobin level normal values 12-16 g/dlEX. Hb level for patient before injury is 15 g/dl after 30 min's of
hemorrhage Hb level will still the same but after 2-3 hrs it'll
decrease 5L the amount of blood in the body after injury Pt'
loses 1ml (same amount of RBC's and Plasma lost so Hb level still
the same) but after 2-3 hrs there'll be reabsorption of fluids from
interstitial space to the intravascular volume (inside the veins) so
this'll increase the plasma more than RBC's and by that Hb level 'll
decrease.
Hematocrit = RBC's
Total Blood
So by increasing the plasma Hematocrit and Hb will decrease.
Hb level isn't a good indicator adequately after the injury but its
benefit after 4 hrs of injuries.
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Hypovolemia (Reduced Blood Volume)
*Can occur as a consequence of a wide variety of pathologicalprocesses. (Traumasevere dehydration, severe vomiting,
severe diarrhea) or Gastric Cancer led to ascites (accumulationof fluids within the peritoneal cavity in abdomen "third
spacing") so this pt' lose blood from intravascular space to
another site either inside or outside the body
*It decreases oxygen transport & increases the risk of tissue
hypoxia & multi organ failure.
*The greater the degree & duration of hypovolemia, the
greater the risk.
*Hypovolemia is divided into THREE categories:
1. Covert compensated hypovolemia
* Is the commonest form but the least often diagnosed
*Hypovolemia is present without very obvious physical signs
(no problems in the history and physical examinations but the
blood volume is less than normal but even that it may appear in
urine analysis a concentrated urinehigh urine osmolarity and
high sodium concentration )
*In conscious patient, CNS symptoms are the best guide
which range from drowsiness & nausea to hiccoughs, thirsty.
*If untreated, patient usually enters the state of overt
compensated hypovolemia.
compensated2. Overt
Due to decreasing in blood volume and blood pressure so there'll
in order to increase bloodactivitysympatheticincreasing inbe
pressure so this will increase heart rate "Tachycardia",
increasing in contractility of heart "pumping activity",
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vasoconstriction in peripheral arteries so they've cold
.particularly hands and feetextremities
Wide arterial pulse pressure (difference between systolic and
diastolic pressures) so hypovolemic pt's 've reflex mechanisms
lead to tachycardia and as a result systolic BP and pulse pressure
will increase.
Urine analysis show*
Increasing in osmolality &
Sodium concentration, in
ABG (Arterial Blood
Gases) they've metabolic acidosis.
* Central venous pressure catheter may be inserted in difficult
cases as normal it ranges between (8-12) but in hypovolemia
it's less than 8, and in overloaded cases (excess fluid in venoussystem) its more than 12.
3. Decompensated hypovolemia
mechanisms are unable to control & maintainProtective*the blood pressure
.shock* This is what is referred to as
in Overt there was hypotension, tachycardia, vasoconstriction,increasing in the contractility of heart to increase BP.
So if the previous mechanisms fail to return the normal BP this
will lead to hypotension and decompensated hypovolemia.
re no longer adequatelya), heart, lungsbrain(organs*Vital
perfused.
Mean arterial pressure falls & may be difficult to record.*
:CNS signs
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Mean arterial pressure = [diastolic BP+ 1/3 (systolic-diastolic)]
Pt' with BP of 120/80 so
MAP= 80 + 1/3(40) = 93.3 mm Hg
* Peripheral pulses are often impalpable (in hypovolemia and
hypotension)
* Blood supply to heart & lungs is compromised which causes
further reduction in cardiac output.
* As myocardial oxygenation becomes critical Tachycardia
changes to bradycardia (in Heart Failure) & level of
consciousness deteriorate.
* If untreated, this condition will progress to total circulatory
arrest.
:Shock
* Shock is described as a clinical syndrome arising from
inadequate tissueperfusion, often complicated by cellular
metabolic dysfunction
*Commonest cause is hypovolemia
* When the mismatch between cardiac output & the metabolic
needs of the patient is great enough, the patient is said to be in
shock.
* Shock is not simply a low blood pressure; low blood pressureis called hypotension which may accompany shock.
Normal BP determined by:
-Contractility of the Heart (Heart Rate)
-Blood volume
So the blood will reach to the cellsadequately with oxygen and eliminate waste
product especially Lactic Acid
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(due to heartInadequate oxygen delivery to meet metabolic demands*
failure, bradycardia and hypovolemia which lead to hypotension).
.metabolic acidosisandhypo perfusionResults in global tissue*
*Shock can occur with a normal blood pressure (normotensive) andhypotension can occur without shock
Ex. Hypertensive Pt' his BP (200/120) with trauma and hemorrhage sohis BP will decrease to (130/80) so this pt' is shocked although the BP is
normal.
Ex. Hypotensive Pt' his normal BP (100/60), (90/50) such as athletes who
are considered as hypotensive pt's, but the pt' has good tissue perfusion so
we can't say he's shocked.
hypotension.of the cases pt' with a shock has severeIN MOST*
Classification of Shock:
1-Decreased circulating volume or decreased preload::
hypotension and shockMI so the heart can't pump blood wellHeart
2-Compromised cardiac function:: Cardiac compressive shock (Extrinsic) pericardiatis "inflammationof pericardium that surround the heart " heart can't expand and contract
wellhypotension and shock
Tension pneumothorax (accumulation of air within pleural cavity)it'll compress over the heart and the heart can't functioning well
hypotension and shock
3-Blood volume abnormality (Hypovolemia)::
a. True hypovolemia pt' with external/internal bleeding ,severe
nausea ,severe vomiting, severe diarrhea dehydration and
hypovolemia.
b. False hypovolemia in vasodilatation case
Ex. Pt' with adrenal insufficiency (not enough amount of cortisol)vasodilatation reduction in BP.
OR : pt' with anaphylactic shock (snake sting) severe dilatation
hypotension and shock.
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hypotension andspinal cord vasodilatationNeurogenic shockshock.
severe vasodilatationsevere infectionshockSeptichypotension and decreased tissue perfusion (shock).
So 1- any disorder lead to vasodilatation will lead to shock
2- Affecting the BV will lead to shock
3-Affecting heart pumping will lead to shock
Pathophysiology of shock:
to the cell is the final commoncritical reduction in oxygen levelA*
pathway leading to shock of all varieties
* Reduced substrate supply & accumulation of the products of cell
metabolism e.g. lactate are contributing factors.
*At cellular level decreased O2 level lead to decrease in level of ATP
(Adenosine triphosphate)
Deficiency of ATP will lead to:
1. Depression of the pump function of the cell with an increase in
intracellular sodium, calcium and water with loss of potassium and
magnesium (Sick cell syndrome)
2. High intracellular calcium >> leads to myocardial cell fatigue, failure
& cardiac arrest.
3. Lactic acidosis which has adverse action on enzyme system of the cell.
Phagocytes will stop functioning*
*Plasma kinins, prostaglandins, leukotrienes are synthesized from the cell
membrane & exert their diverse effects on circulation.
*Neutrophils are stimulated to produce elastase which is very injurious to
pneumocytes (lung cells) resulting in ARDS (Acute Respiratory DistressSyndrome) fatal
*Stimulation of the coagulation pathway will lead to consumptive
coagulopathy resulting in disseminated intravascular coagulation DIC (Pt'
with bleeding tendency and thrombosis tendency at the same time)fatal
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*All the systems of the body are affected leading to MODS (Multi Organ
Dysfunction Syndrome)Progression of physiologic effects as shockensues:
Cardiac depression
Respiratory distress
Renal failure
DIC
Result is end organ failure
Inadequate systemic oxygen delivery activates autonomic responses
to maintain systemic oxygen delivery:
1- Sympathetic nervous system
NE, epinephrine, dopamine, and cortisol release.*
*Causes vasoconstriction, increase in HR, and increase of cardiac
contractility (cardiac output).
2- Renin-angiotensin axis
* Water and sodium conservation and vasoconstriction.
*Increase in blood volume and blood pressure.
irculation )Creathing,Birway,(AABCs
Cardio respiratory monitor (ECG, heart rate, respiratory rate to monitor
the Pt')
Pulse oximetry HR, O2 saturation > 92% normally but in hypoxia it's
less than that.
Supplemental oxygen facemask
IV access Canula
ABG, labs blood cross match (need 30-45 min's) its long time so we
give the pt' IV fluids (crystalloids = Normal Saline)
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Foley catheter to monitor urine output
Vital signs BP, HR
(VS, mental status, skin color, temperature, pulses, etc)Physical exam
Ex. Hypovolic shock pt' tachycardia , hypotension , confusion,
seizures "in severe cases", vasoconstriction in non vital organs "skin,
GIT, muscles " so cold and blue hands and feet .
Do you remember how to quickly
estimate blood pressure by pulse?
If you palpate a pulse:
Radial artery at least 70 mm Hg
Foot at least 90 mm Hg
60
80
90
70
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Hypovolemia also classified to:
1-Mild < 20% pallor, cold extremities, delayed capillary refill,
collapsed veins, tachycardia.
2-Moderate 20-40% same signs for mild plus oliguria "decreased urineoutput", postural hypotension.
3-Severe >40% same signs plus mental status changes "confusion,
seizures, anxiety"
:Goals of Treatment
ABCDE
AirwayControl work ofBreathing
optimize Circulation
assure adequate oxygen Delivery
Achieve End points of resuscitation
1- Airway*Determine need for intubation "endotracheal tube".
* Control Work of Breathing
Respiratory muscles consume a significant amount of oxygen : if we
make Mechanical ventilation for the pt' this will supply O2 to him so
this oxygen will reach to the brain,lungs,heart so this will improve the
survival in severe shock.
2- Optimizing Circulation
* We give the pt' IV fluids (crystalloids = Normal Saline) while we're
waiting for blood group test then we watch the pt' after IV fluids
supplying.
* CVP "Central Venous Pressure" 8-12 mm Hg.
* Urine output 0.5 ml/kg/hr (30 ml/hr): in hypovolemia it'll be less thanthat.
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* Improving heart rate > 100 in hypovolemia "tachycardia".
3- Maintaining Oxygen Delivery
* We can transport blood to the pt' to increase Hb level.* Decrease oxygen demands.
* Provide analgesia and anxiolytics to relax muscles and avoid
shivering.
4- End Points of Resuscitation
Goal directed approach*
Urine output > 0.5 ml/kg/hr
CVP 8-12 mmHg
MAP 65 to 90 mmHg
Pharmacological Agents:
If restoration of blood volume, red cell mass, & adequate oxygenation fail
to restore an adequate cardiac output & oxygen delivery then
pharmacological agents may be required.
Dopamine improves the cardiac output & urine output so this will
increase BP.
Dobutamine acting directly on B1-adrenergic receptors has moreinotropic action on the heart.
Persistent Hypotension:
Inadequate volume resuscitation
Pneumothorax (accumulation of air in pleural cavity) not improved
by giving IV fluids.
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Cardiac tamponade (accumulation of blood or fluids around the heart)
Hidden bleeding (internal bleeding)
Adrenal insufficiency
Medication allergy
I tried my best in this script but the lecture too onerous.
Forgive me for any mistake
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