Hemorrhage is classified according to :

Source
Time of onset Site of bleeding

1. Arterial hemorrhage Bright red blood Spurting as a jet which rises & falls with the pulse. 2. Venous bleeding Darker red. Steady & copious flow. 3. Capillary bleeding Bright red often rapid ooze.

1. Primary hemorrhage: Occurs at the time of injury or operation.

2. Reactionary hemorrhage

3. Secondary hemorrhage

follow primary hemorrhage within 24hours (Usually 4-6) hours. Mainly due to slipping of a ligature, dislodgment of a clot or cessation of reflex vasospasm. Precipitating factors are :
i. Rise in blood pressure. ii. Refilling of the venous system on recovery from shock iii. Restlessnes, coughing & vomiting which raise the

venous pressure.(bleeding after thyroidectomy)

Occurs 7-14 days after injury

Predisposing factors are
1. Pressure of a drainage tube 2. Ligature in infected area. 3. Cancer.

I.

External hemorrhage:
- Is visible & is called revealed hemorrhage.

II.

Internal hemorrhage:
- Is invisible & is concealed hemorrhage as in ruptured spleen or liver, fracture femur, ruptured ectopic gestation.

Concealed hemorrhage may become revealed as in hematemesis & melena or hematuria in ruptured kidney.

Total blood volume can be derived from patients weight : Infants 80-85ml\kg Adults 65-75ml/kg

Measuring blood loss 1. Blood clot the size of fist is roughly equal to 500ml. 2. Swelling in closed fractures
Moderate swelling in closed fracture of the tibia equals

500-1500ml blood loss. Moderate swelling in closed fracture of femur 500-2000ml blood loss.

3. On the operation table :

Swab weighing , blood loss can be measured by weighing swabs after use & subtracting the dry weight. (1gm=1ml) Measuring the blood collected in the suction & drainage bottles. In big extensive operations keep in mind evaporation & sweating . for e.g in radical mastectomy or partial gastrectomy multiply the swab weighing total by 1.5 & for more prolonged operations via large wounds such as abdominothoracic or abdomino-perineal operations multiply by 2.

4. Hemoglobin level.

This is estimated in g/100ml or g/dl. normal values 12-16 g/dl There will be no immediate change after some hours , the level falls as a result of the influx of interstitial fluid.

Can occur as a consequence of a wide variety of pathological processes.

Is an acute medical emergency.

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.

Is the commonest form but the least often diagnosed. Hypovolemia is present without very obvious physical signs. It is very difficult to diagnose In conscious patient ,CNS symptoms are the best guide which range from drowsiness & nausea to hiccoughs Any thirsty patient should be considered hypovolemic.

Urine analysis show increase osmolality & sodium concentration both are considered to be the most useful laparatory investigations. Although it is very common, most patients withstand the insult If untreated patient usually enters the state of overt compensated hypovolemia

Blood pressure is maintained still. Hypovolemia is present to an extent that reflex mechanisms are required to maintain supply to vital organs & this is obvious clinically. History is very important & on examination there is increase sympathetic drive such as tachycardia; increased systolic pressure. Wide arterial pulse pressure, cool skin particularly hands and feet. CNS signs as drowsiness, confusion & an increased respiratory rate.

In acute phase most laparatory investigations are of little use. Arterial blood gas analysis can be done rapidly ; hypovolemic patients are hypoxic & may have metabolic acidosis. Urine analysis may support the diagnosis but no single test is diagnostic. Cenratl venous pressure catheter may be inserted in difficult cases

This is what is refered to as shock. Protective mechanisms are unable to control & maintain the blood pressure Vital organs are no longer adequately perfused Mean arterial pressure falls & may be difficult to record Peripheral pulses are often impalpable.

Blood supply to heart & lungs is compromised which causes further reduction in cardiac out put . As myocardial oxygenation becomes critical Tachycardia changes to bradycardia & level of conscioussnes deteriorate. If untreated ,this condition will progress to total circulatory arrest.

Shock is Described as a clinical syndrome arising from inadequate tissue perfusion, often complicated by cellular metabolic dysfunction. When the mismatch between cardiac out put & 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 pressure is called hypotension which may accompany shock .

 Inadequate oxygen delivery to meet metabolic demands Results in global tissue hypoperfusion and metabolic acidosis Shock can occur with a normal blood pressure and hypotension can occur without shock

1.

Decreased circulating volume or decreased preload

True Hypovolemia
Blood loss Plasma loss Dehydration

Apparent hypovolemia (vasodilatation)

Adrenal insuficiency Anaphylaxis Neurogenic factors Sepsis

2.

Compromised cardiac function

Cardiac compressive shock (Extrinsic) Cardiogenic shock (intrinsic)

A critical reduction in oxygen level to the cell is the final common pathway leading to shock of all varities 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)
High intracellular calcium >> leads to myocardial cell fatigue, failure & cardiac arrest. Lactic acidosis which has adverse action on enzyme system of the cell.

2.

3.

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 resulting in ARDS Stimulation of the coagulation pathway will lead to consumptive coagulopathy resulting in disseminated intravascular coagulation DIC All the systems of the body are affected leading to MODS (Multi organ dysfunction syndrome)

 Progression of physiologic effects as shock ensues

Cardiac depression Respiratory distress Renal failure DIC

Result is end organ failure

 Inadequate systemic oxygen delivery activates autonomic responses to maintain systemic oxygen delivery
Sympathetic nervous system
NE, epinephrine, dopamine, and cortisol release
Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac output)

Renin-angiotensin axis
Water and sodium conservation and vasoconstriction Increase in blood volume and blood pressure

 ABCs
Cardiorespiratory monitor Pulse oximetry Supplemental oxygen IV access ABG, labs Foley catheter Vital signs

 Physical exam (VS, mental status, skin color, temperature, pulses, etc) Infectious source Labs:
CBC Chemistries Lactate Coagulation studies Cultures ABG

Lumbar puncture Wound cultures Acute abdominal series Abdominal/pelvic CT or US Cortisol level Fibrinogen, FDPs, D-dimer

 Physical examination
Vital Signs CNS mental status

Skin color, temp, rashes, sores

CV JVD, heart sounds Resp lung sounds, RR, oxygen sat, ABG GI abd pain, rigidity, guarding, rebound Renal urine output

 Do you remember how to quickly estimate blood pressure by pulse? If you palpate a pulse, you know SBP is at least this number

60

70 80

90

Mild <20% vol. loss Pallor Cool extremities Capillary refill Collapsed veins Tachycardia

Moderate20-40% Pallor Cool extremities Capillary refill Collapsed veins Tachycardia Oliguria Postural hypotension

Severe>40%vol loss Pallor Cool extremities Capillary refill Collapsed veins Tachycardia Oligourea Postural hypotension Mental status changes Agitation Restlessness

Hemorrhage of less than 20% of circulating blood volume causes little or no alteration in blood pressure & heart rate. As more volume is lost and more rapid ;signs are more prominent

 ABCDE
Airway control work of Breathing optimize Circulation assure adequate oxygen Delivery achieve End points of resuscitation

 Determine need for intubation but remember: intubation can worsen hypotension
Sedatives can lower blood pressure Positive pressure ventilation decreases preload

 Respiratory muscles consume a significant amount of oxygen Tachypnea can contribute to lactic acidosis

Mechanical ventilation and sedation decrease WOB and improves survival

 Isotonic crystalloids
Titrated to:
CVP 8-12 mm Hg
Urine output 0.5 ml/kg/hr (30 ml/hr) Improving heart rate

May require 4-6 L of fluids

 Decrease oxygen demands

Provide analgesia and anxiolytics to relax muscles and avoid shivering

Maintain arterial oxygen saturation/content

Give supplemental oxygen Maintain Hemoglobin > 10 g/dL

Serial lactate levels or central venous oxygen saturations to assess tissue oxygen extraction

 Goal of resuscitation is to maximize survival and minimize morbidity Use objective hemodynamic and physiologic values to guide therapy Goal directed approach
Urine output > 0.5 mL/kg/hr CVP 8-12 mmHg MAP 65 to 90 mmHg Central venous oxygen concentration > 70%

If restoration of blood volume, red cell mass, & adequate oxygenation fail to restore an adequate cardiac out put & oxygen delivery then pharmacological agents may be required. Dopamine improves the cardiac output & urine output Dobutamine acting directly on B1-adrenergic receptors has more inotropic action on the heart.

Inadequate volume resuscitation Pneumothorax Cardiac tamponade Hidden bleeding Adrenal insufficiency Medication allergy

 Two or more of SIRS criteria

Temp > 38 or < 36 C HR > 90 RR > 20 WBC > 12,000 or < 4,000

Plus the presumed existence of infection Blood pressure can be normal!

 Sepsis (remember definition?) Plus refractory hypotension

After bolus of 20-40 mL/Kg patient still has one of the following:

SBP < 90 mm Hg MAP < 65 mm Hg Decrease of 40 mm Hg from baseline

Nguyen H et al. Severe Sepsis and Septic-Shock: Review of the Literature and Emergency Department Management Guidelines. Ann Emerg Med. 2006;42:28-54.

 Clinical signs:
Hyperthermia or hypothermia Tachycardia Wide pulse pressure Low blood pressure (SBP<90) Mental status changes

Beware of compensated shock!

Blood pressure may be normal

Cardiac monitor Pulse oximetry CBC, Biochem. labs, coags, LFTs, lipase, UA ABG with lactate Blood culture x 2, urine culture CXR Foley catheter (why do you need this?)

 2 large bore IVs

NS IVF bolus- 1-2 L wide open (if no contraindications)

Supplemental oxygen Empiric antibiotics, based on suspected source, as soon as possible

 Antibiotics- Survival correlates with how quickly the correct drug was given Cover gram positive and gram negative bacteria
Zosyn 3.375 grams IV and ceftriaxone 1 gram IV or Imipenem 1 gram IV

Add additional coverage as indicated

Pseudomonas- Gentamicin or Cefepime MRSA- Vancomycin Intra-abdominal or head/neck anaerobic infectionsClindamycin or Metronidazole Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae Neutropenic Cefepime or Imipenem

 If no response after 2-3 L IVF, start a vasopressor (norepinephrine, dopamine, etc) and titrate to effect Goal: MAP > 60 Consider adrenal insufficiency: hydrocortisone 100 mg IV