EMERGENCY MEDICINE SYSTEM

Name : Muhammad Nizamuddin Bin Othman

NIM : 060100259

Semester : VI ( Sixth)

Facilitator : dr. Nurchaliza Hazaria Siregar, Sp.M

Tutorial Group : A3

FACULTY OF MEDICINE

UNIVERSITY SUMATERA UTARA

2008

Content

Preface……………………………………………………………….……………

Trigger…………………………………………………………………………….

Objective of Learning……………………………………………….……………

The Questions…………….......……………………………………..…………….

The Answers………………………………………………………..……………..

Explanation…………………………………………………..……..……………

Conclusion………………………………………………………….…………….

References…………………………………..………………………..…………...

Preface

I gratefully acknowleged the fasilitator, dr. Nurchaliza Hazaria Siregar, SpM

who facilitated our tutorial excellently. And not forgotten, group members of A3 who

have been a big help in finishing this paper. In this report, the case that I will discuss

is about hypovolemic shock. A man aged 60 years old comes to the ICU of Haji

Adam Malik Hospital with symptoms of restless and hard to breath. From what I had

learned, we must discuss everything that might be the underlying causes of the

symptoms, as the disease might deteriorate and endangering the patient life. I will

discuss it beginning with the basic science of human health until the disease itself.

Below are the learning issues that will be discussed in this report:

1. All about Hypovolemic Shock

2. Initial assessment in emergency cases ( Primary and secondary survey)

3. ICU admission criteria

4. All about hemopneumothorac and pneumothorac.

5. Bioethic aspect in emergency.

Thank you for the intention.

16th May 2009

( )

Block’s name: Emergency Medicine System

Fasilitator: dr. Nurchaliza Hazaria Siregar, SpM

Data of Implementation:

a) Date of tutorial: 2nd April 2009 ( 1st tutorial), 6th April 2009 ( 2nd tutorial)

b) Venue : A3 tutorial room

c) First stimulant & more info

d) Time: 07.00 – 09.30 WIB ( 1st tutorial), 13.00 – 15.30 WIB (2nd tutorial)

e) Venue: Tutorial Hall of Seminar.

Trigger :

A 60 years old male admitted to ICU RSUP H Adam Malik with complaints of

dyspnea and restlessness. The symptoms occur since 3 hours ago after he had a traffic

accident. During the accident, he had a contusion at right side of his chest. Besides

that, he had an open wound with obtrusive right thigh bone.

More info I :

Further examination after primary resuscitation to patient:

- Blood laboratory :

Full Blood Count: Hb 8 gr%, Ht 26, Leukocyte 12.800/mm3 , Thrombocyte

200.000/mm3. Urine: Dark yellow. Blood Gas Analysis : pH: 7,125, pCO2 :

60, pO2 : 50, HCO3- : 10, BD : -10, SaO2 : 88%. Electrolyte : Na/K/Cl :

140/4/95. Blood Glucose ad random : 300 mg/dl

- ECG 12 leads : sinus tachycardia

- AP Thorax X-ray : Right sided hemopneumothorax , fracture of 3,4,5 frontal

ribs, air fluid level can be seen, mediastinum shifts to the left, increase

bronchovascular at left lung. Femur X-Ray : fracture at 1/3 middle femur bone

and head scanning : in normal range.

From allo anamnesis, the patient admitted that he went to Pulmonary

Department RSUHAM for regular treatment because he always has trouble

breathing. He also admitted that he was using inhaler and smoke 20 cigarettes

per day.

More Info II

For hemopneumothorax treatment, doctor suggested that he will use Water Sealed

Drainage (WSD) to the patient. The doctor had explained the purpose and procedure

of WSD to the patient and his family but the family didn’t approved WSD.

How is your reaction to the family’s decision not to approved WSD to the patient?

Objective of Learning

A. Understand the pathophysiology of hypovolemic shock

B. Understand about initial assessment and management during emergency

C. Understand about hemopneumothorax and pneumothorax

D. Understand the admission criteria to ICU

E. Understand the bioethics aspects in emergency

Questions

1. How does the hypovolemic shock happens?

2. What is initial assessment and management during emergency?

3. What are the difference between hemopneumothorax and pneumothorax?

4. What are the criteria for admission to the ICU?

5. What are the bioethics aspects in emergency?

Answer:

A. All About Hypovolemic Shock

Background

Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate circulating volume and subsequent inadequate perfusion. Most often, hypovolemic shock is secondary to rapid blood loss (hemorrhagic shock).

Acute external blood loss secondary to penetrating trauma and severe GI bleeding disorders are 2 common causes of hemorrhagic shock. Hemorrhagic shock can also result from significant acute internal blood loss into the thoracic and abdominal cavities.

Two common causes of rapid internal blood loss are solid organ injury and rupture of an abdominal aortic aneurysm. Hypovolemic shock can result from significant fluid (other than blood) loss. Two examples of hypovolemic shock secondary to fluid loss include refractory gastroenteritis and extensive burns.

Pathophysiology

The human body responds to acute hemorrhage by activating the following major physiologic systems: the hematologic, cardiovascular, renal, and neuroendocrine systems.

The hematologic system responds to an acute severe blood loss by activating the coagulation cascade and contracting the bleeding vessels (by means of local thromboxane A2 release). In addition, platelets are activated (also by means of local thromboxane A2 release) and form an immature clot on the bleeding source. The damaged vessel exposes collagen, which subsequently causes fibrin deposition and stabilization of the clot. Approximately 24 hours are needed for complete clot fibrination and mature formation.

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

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

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

History

In a patient with possible shock secondary to hypovolemia, the history is vital in determining the possible causes and in directing the workup. Hypovolemic shock secondary to external blood loss typically is obvious and easily diagnosed. Internal bleeding may not be as obvious as patients may complain only of weakness, lethargy, or a change in mental status.

Symptoms of shock, such as weakness, lightheadedness, and confusion, should be assessed in all patients.

In the patient with trauma, determine the mechanism of injury and any information that may heighten suspicion of certain injuries (eg, steering wheel damage or extensive passenger compartment intrusion in a motor vehicle accident).

If conscious, the patient may be able to indicate the location of pain.

Vital signs, prior to arrival in the ED, should also be noted.

Chest, abdominal, or back pain may indicate a vascular disorder.

The classic sign of a thoracic aneurysm is a tearing pain radiating to the back. Abdominal aortic aneurysms usually result in abdominal, back pain, or flank pain.

In patients with GI bleeding, inquiry about hematemesis, melena, alcohol drinking history, excessive nonsteroidal anti-inflammatory drug use, and coagulopathies (iatrogenic or otherwise) is very important.

If a gynecologic cause is being considered, gather information about the following: last menstrual period, risk factors for ectopic pregnancy, vaginal bleeding (including amount and duration), vaginal passage of products of conception, and pain. All women of childbearing age should undergo a pregnancy test, regardless of whether they believe that they are pregnant. A negative pregnancy test typically excludes ectopic pregnancy as a diagnosis.

Causes

The causes of hemorrhagic shock are traumatic, vascular, GI, or pregnancy related.

Traumatic causes can result from penetrating and blunt trauma. Common traumatic injuries that can result in hemorrhagic shock include the following: myocardial laceration and rupture, major vessel laceration, solid abdominal organ injury, pelvic and femoral fractures, and scalp lacerations.

Vascular disorders that can result in significant blood loss include aneurysms, dissections, and arteriovenous malformations.

GI disorders that can result in hemorrhagic shock include the following: bleeding esophageal varices, bleeding peptic ulcers, Mallory-Weiss tears, and aortointestinal fistulas.

Pregnancy-related disorders include ruptured ectopic pregnancy, placenta previa, and abruption of the placenta. Hypovolemic shock secondary to an ectopic pregnancy is common. Hypovolemic shock secondary to an ectopic pregnancy in a patient with a negative urine pregnancy test is rare but has been reported.

Physical Examination

The physical examination should always begin with an assessment of the airway, breathing, and circulation. Once these have been evaluated and stabilized, the circulatory system should be evaluated for signs and symptoms of shock.

Do not rely on systolic BP as the main indicator of shock; this practice results in delayed diagnosis. Compensatory mechanisms prevent a significant decrease in systolic BP until the patient has lost 30% of the blood volume. More attention should be paid to the pulse, respiratory rate, and skin perfusion. Also, patients taking beta-blockers may not present with tachycardia, regardless of the degree of shock.

Classes of hemorrhage have been defined, based on the percentage of blood volume loss. However, the distinction between these classes in the hypovolemic patient often is less apparent. Treatment should be aggressive and directed more by response to therapy than by initial classification.

Class I hemorrhage (loss of 0-15%) o In the absence of complications, only minimal tachycardia is seen.

o Usually, no changes in BP, pulse pressure, or respiratory rate occur.

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

Class II hemorrhage (loss of 15-30%)

o Clinical symptoms include tachycardia (rate >100 beats per minute), tachypnea, decrease in pulse pressure, cool clammy skin, delayed capillary refill, and slight anxiety.

o The decrease in pulse pressure is a result of increased catecholamine levels, which causes an increase in peripheral vascular resistance and a subsequent increase in the diastolic BP.

Class III hemorrhage (loss of 30-40%)

o By this point, patients usually have marked tachypnea and tachycardia, decreased systolic BP, oliguria, and significant changes in mental status, such as confusion or agitation.

o In patients without other injuries or fluid losses, 30-40% is the smallest amount of blood loss that consistently causes a decrease in systolic BP.

o Most of these patients require blood transfusions, but the decision to administer blood should be based on the initial response to fluids.

Class IV hemorrhage (loss of >40%)

o Symptoms include the following: marked tachycardia, decreased systolic BP, narrowed pulse pressure (or immeasurable diastolic pressure), markedly decreased (or no) urinary output, depressed mental status (or loss of consciousness), and cold and pale skin.

o This amount of hemorrhage is immediately life threatening.

In the patient with trauma, hemorrhage usually is the presumed cause of shock. However, it must be distinguished from other causes of shock. These include cardiac tamponade (muffled heart tones, distended neck veins), tension pneumothorax (deviated trachea, unilaterally decreased breath sounds), and spinal cord injury (warm skin, lack of expected tachycardia, neurological deficits).

The 4 areas in which life-threatening hemorrhage can occur are as follows: chest, abdomen, thighs, and outside the body.

o The chest should be auscultated for decreased breath sounds, because life-threatening hemorrhage can occur from myocardial, vessel, or lung laceration.

o The abdomen should be examined for tenderness or distension, which may indicate intraabdominal injury.

o The thighs should be checked for deformities or enlargement (signs of femoral fracture and bleeding into the thigh).

o The patient's entire body should then be checked for other external bleeding.

In the patient without trauma, the majority of the hemorrhage is in the abdomen. The abdomen should be examined for tenderness, distension, or bruits. Look for evidence of an aortic aneurysm, peptic ulcer disease, or liver congestion. Also check for other signs of bruising or bleeding.

In the pregnant patient, perform a sterile speculum examination. However, with third-trimester bleeding, the examination should be performed as a "double set-up" in the operating room. Check for abdominal, uterine, or adnexal tenderness.

Prehospital Care

The treatment of patients with hypovolemic shock often begins at an accident scene or at home. The prehospital care team should work to prevent further injury, transport the patient to the hospital as rapidly as possible, and initiate appropriate treatment in the field. Direct pressure should be applied to external bleeding vessels to prevent further blood loss.

Prevention of further injury applies mostly to the patient with trauma. The cervical spine must be immobilized, and the patient must be extricated, if applicable, and moved to a stretcher. Splinting of fractures can minimize further neurovascular injury and blood loss.

Although in selected cases stabilization may be beneficial, rapid transport of sick patients to the hospital remains the most important aspect of prehospital care. Definitive care of the hypovolemic patient usually requires hospital, and sometimes surgical, intervention. Any delay in definitive care, eg, such as delayed transport, is potentially harmful.

Most prehospital interventions involve immobilizing the patient (if trauma is involved), securing an adequate airway, ensuring ventilation, and maximizing circulation.

o In the setting of hypovolemic shock, positive-pressure ventilation may diminish venous return, diminish cardiac outcome, and worsen the shock state. While oxygenation and ventilation are necessary, excessive positive-pressure ventilation can be detrimental for a patient suffering hypovolemic shock.

o Appropriate treatment usually can be initiated without delaying transport. Some procedures, such as starting intravenous (IV) lines or splinting of extremities, can be performed while a patient is being extricated. However, procedures in the field that prolong transportation should be delayed. Benefits to giving IV fluids prior to departure from the scene are not clear; however, IV lines and fluid resuscitation should be started and continued once the patient is en route to definitive care.

In recent years, there has been considerable debate regarding the use of military antishock trousers (MAST). By the 1980s, the American College of Surgeons Committee on Trauma included their use in the standard of care for all patients with trauma and signs or symptoms of shock. Since that time, studies have failed to show improved outcome with the use of MAST. The American College of Surgeons Committee on Trauma no longer recommends the use of MAST.

Emergency Department Care

Three goals exist in the emergency department treatment of the patient with hypovolemic shock as follows: (1) maximize oxygen delivery - completed by ensuring adequacy of ventilation, increasing oxygen saturation of the blood, and restoring blood flow, (2) control further blood loss, and (3) fluid resuscitation. Also, the patient's disposition should be rapidly and appropriately determined.

Maximizing oxygen delivery

o The patient's airway should be assessed immediately upon arrival and stabilized if necessary. The depth and rate of respirations, as well as breath sounds, should be assessed. If pathology (eg, pneumothorax, hemothorax, flail chest) that interferes with breathing is found, it should be addressed immediately. High-flow supplemental oxygen should be administered to all patients, and ventilatory support should be given, if needed. Excessive positive-pressure ventilation can be detrimental for a patient suffering hypovolemic shock and should be avoided.

o Two large bore IV lines should be started. The Poiseuille law states that flow is inversely related to the length of the IV catheter and directly related to its radius to the fourth power. Thus, a short large-caliber IV catheter is ideal; the caliber is much more significant than the length. IV access may be obtained by means of percutaneous access in the antecubital veins, cutdown of saphenous or arm veins, or access in the central veins by using the Seldinger technique. If central lines are obtained, a large-bore single-lumen catheter should be used. The most important factor in determining the route of access is the practitioner's skill and experience.

o Placement of an arterial line should be considered for patients with severe hemorrhage. For these patients, the arterial line will provide continuous blood pressure monitoring and also ease arterial blood gas testing.

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

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

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

o The position of the patient can be used to improve circulation; one example is raising the hypotensive patient's legs while fluid is being given. Another example of useful positioning is rolling a hypotensive gravid patient with trauma onto her left side, which displaces the fetus from the inferior vena cava and increases circulation. The Trendelenburg position is no longer recommended for hypotensive patients, as the patient is predisposed to aspiration. In addition, the Trendelenburg position does not improve cardiopulmonary performance and may worsen gas exchange.

o Autotransfusion may be a possibility in some patients with trauma. Several devices that allow for the sterile collection, anticoagulation, filtration, and

retransfusion of blood are available. In the trauma setting, this blood almost always is from a hemothorax collected by means of tube thoracostomy.

Controlling further blood loss o Control of further hemorrhage depends on the source of bleeding and often

requires surgical intervention. In the patient with trauma, external bleeding should be controlled with direct pressure; internal bleeding requires surgical intervention. Long-bone fractures should be treated with traction to decrease blood loss.

o In the patient whose pulse is lost in the ED or just prior to arrival, an emergency thoracotomy with cross-clamping of the aorta may be indicated to preserve blood flow to the brain. This procedure is palliative at best and requires immediate transfer to the operating room.

o In the patient with GI bleeding, intravenous vasopressin and H2 blockers have been used. Vasopressin commonly is associated with adverse reactions, such as hypertension, arrhythmias, gangrene, and myocardial or splanchnic ischemia. Therefore, it should be considered secondary to more definitive measures. H2 blockers are relatively safe but have no proven benefit.

o Somatostatin and octreotide infusions have been shown to reduce gastrointestinal bleeding from varices and peptic ulcer disease. These agents possess the advantages of vasopressin without the significant side effects.

o In patients with variceal bleeding, use of a Sengstaken-Blakemore tube can be considered. These devices have a gastric balloon and an esophageal balloon. The gastric one is inflated first, and then the esophageal one is inflated if bleeding continues. The use of this tube has been associated with severe adverse reactions, such as esophageal rupture, asphyxiation, aspiration and mucosal ulceration. For this reason, its use should be considered only as a temporary measure in extreme circumstances.

o Virtually all causes of acute gynecological bleeding that cause hypovolemia (eg, ectopic pregnancy, placenta previa, abruptio placenta, ruptured cyst, miscarriage) require surgical intervention.

o Early consultation and definitive care are the keys. The goal in the ED is to stabilize the hypovolemic patient, determine the cause of bleeding, and provide definitive care as quickly as possible. If transfer to another hospital is necessary, resources should be mobilized early.

o In patients with trauma, if the emergency medical services personnel indicate potential serious injury, the surgeon (or trauma team) should be notified prior to the patient's arrival. In a 55-year-old patient with abdominal pain, for example, emergency ultrasonography of the abdomen may be necessary to identify an abdominal aortic aneurysm before the vascular surgeon is notified. Every patient should be individually evaluated, because delaying definitive care can increase morbidity and mortality.

Whether crystalloids or colloids are best for resuscitation continues to be a matter for discussion and research. Many fluids have been studied for use in

resuscitation; these include isotonic sodium chloride solution, lactated Ringer solution, hypertonic saline, albumin, purified protein fraction, fresh frozen plasma, hetastarch, pentastarch, and dextran 70.

o Proponents of colloid resuscitation argue that the increased oncotic pressure produced with these substances decreases pulmonary edema. However, the pulmonary vasculature allows considerable flow of material, including proteins, between the intravascular space and interstitium. Maintenance of the pulmonary hydrostatic pressure at less than 15 mm Hg appears to be a more important factor in preventing pulmonary edema.

o Another argument is that less colloid is needed to increase the intravascular volume. Studies have shown this to be true. However, they still have not demonstrated any difference in outcome with colloids compared with crystalloids.

o Synthetic colloid solutions, such as hetastarch, pentastarch, and dextran 70, have some advantages compared with natural colloids such as purified protein fraction, fresh frozen plasma, and albumin. They have the same volume-expanding properties, but because of their structures and high molecular weights, they remain mostly in the intravascular space, reducing the occurrence of interstitial edema. Although theoretic advantages exist, studies have failed to show a difference in ventilatory parameters, pulmonary function test results, days using a ventilator, total hospital days, or survival.

o The combination of hypertonic saline and dextran also has been studied because of previous evidence that it may improve cardiac contractility and circulation. Studies in the US and Japan have failed to show any difference when this combination was compared with isotonic sodium chloride solution or lactated Ringer solution. Thus, despite the many available resuscitation fluids, current recommendations still advocate the use of normal saline or lactated Ringer solution. In the US, one reason for the predominant use of crystalloids over the other resuscitative fluids is cost.

Another area of interest regarding resuscitation is whether the goal should be to restore normal circulating volume and BP prior to definitive control of bleeding.

o Findings from early studies showed that animals that were bled had increased survival if they received fluid resuscitation. However, in these studies, bleeding was well controlled with ligation after the animals were bled.

o During the Korean and Vietnam wars, much more aggressive fluid resuscitation, as well as rapid access to definitive care, was emphasized. It was noted that patients who were aggressively resuscitated tended to have better outcomes, and in the 1970s, these principles were widely adopted in civilian patients.

o Since then, many studies have been conducted to determine if these principles are valid in patients with uncontrolled hemorrhage. Most of

these studies revealed increased survival in the permissive hypotension or delayed treatment arms. The theory is that increased pressure causes more bleeding and disrupts initial clots, whereas extreme hypotension may increase the risk of cerebral perfusion.

o The questions that have not been answered adequately are as follows: Which mechanisms and injury patterns are more amenable to the restoration of circulating blood volume? What BP is adequate but not excessive?

o Although some data indicate that a systolic BP of 80-90 mm Hg may be adequate in penetrating truncal trauma without head injury, further studies are needed.

o Current recommendations are for aggressive fluid resuscitation with lactated Ringer solution or normal saline in all patients with signs and symptoms of shock, regardless of underlying cause.

B. Initial Assessment in Emergency Cases

PRIMARY SURVEY

As stated earlier, the primary survey is a process carried  out  to  detect  and treat   life-threatening conditions. As these conditions are detected, lifesaving measures are taken immediately, and early transport may be initiated. The information acquired before and upon your arrival on the scene provides you with a  starting  point  for  the  primary survey. The primary survey is a “treat-as-you-go” process. As each major problem is detected, it is treated immediately, before moving on to the next. During   the   primary survey, you should be concerned with what are referred to as the ABCDEs of emergency care: airway, breathing, circulation, disability, and expose.

A=Airway.

An  obstructed  airway  may  quickly lead to respiratory arrest and death. Assess responsiveness   and,   if necessary, open the airway.

B=Breathing.

Respiratory  arrest  will  quickly  lead to  cardiac  arrest.   Assess  breathing, and,   if   necessary,   provide   rescue breathing. Look   for   and   treat conditions   that   may   compromise breathing,   such   as   penetrating trauma to the chest.

C=Circulation. If  the  patient’s  heart  has  stopped,blood and oxygen are not being sent to  the  brain. Irreversible  changes will begin to occur in the brain in 4 to 6  minutes;  cell  death  will  usually occur  within  10  minutes. Assess circulation,   and,   if   necessary, provide  cardiopulmonary  resuscita- tion (CPR).   Also check for profuse bleeding   that   can   be   controlled.

Assess   and   begin   treatment   for severe  shock  or  the  potential  for severe shock.

D=Disability.

Serious   central   nervous   system injuries can lead to death.  Assess the patient’s level of consciousness and, if you suspect a head or neck injury, apply a rigid neck collar. Observe the neck before you cover it up. Also do a quick assessment of the patient’s ability to move all extremities.

E=Expose.

You cannot treat conditions you have not  discovered. Remove clothing especially if the patient is not alert or communicatin with you–to see if you   missed   any   life-threatening injuries. Protect   the   patient’s privacy, and keep the patient warm with a blanket if necessary. As soon as the ABCDE process is completed, you will need to make what is referred to as a status decision of the patient’s condition. A status decision is a judgment about the severity of the patient’s condition and whether the patient requires immediate transport to a medical facility without a secondary survey at the scene. Ideally, the ABCDE steps, status, and transport decision  should  be  completed within  10  minutes  of your arrival on the scene.

SECONDARY SURVEY

The  object of a secondary survey is to detect medical and injury-related problems that do not pose an immediate threat to survival but that, if left untreated, may do so. Unlike the primary survey, the secondary survey is not a “treat-as-you-go” process. Instead,  you  should  mentally note the injuries and problems as you systematically complete the survey.Then yo  must formulate priorities and a plan for treatment. The secondary survey for a patient who presents with medical illness is somewhat different from that of an injured patient.Usually the trauma assessment is about  20  percent patient interview and 80 percent physical exam. On the other hand,the medical assessment is 80 percent patient interview and 20 percent physical exam. Both the physical exam and patient interview should always be done for all medical and trauma patients.

C. ICU Admission Criteria

Admission Criteria

ICU admission criteria should select patients who are likely to benefit from ICU care. ICU care has been demonstrated to improve outcomes in severely ill, unstable patient populations.

ICU practitioners should understand tools for assessing severity of illness and prognosis of critically ill patients.

Existing predictive instruments have only been applied to patients already admitted to an ICU and have not been tested as preadmission screening tools.

Both extremes of the risk of death spectrum are not ideal ICU patients: those “too well to benefit” and those “too sick to benefit.”

o Defining these groups may be difficult solely based on diagnosis

o Criteria defining “substantial benefit” are subject to interpretation

Prioritization Model

Priority 1:

Unstable patients in need of intensive treatment and monitoring that cannot be provided outside of the ICU.This includes ventilator support and vasoactive drug infusions. Priority 1 patients have no limits placed on the extent of therapy they are to receive.

Priority 2:

Patients requiring intensive monitoring and potential for immediate intervention. No therapeutic limits are stipulated for these patients.

Priority 3:

Unstable critically ill patients who have a reduced likelihood of recovery because of underlying disease or the nature of their acute illnessPatients may receive intensive treatment to relieve acute illness but limits on therapeutic efforts may be set, such as no intubation or resuscitation.

Priority 4:

Patients who are generally not appropriate for ICU admission Admission of these patients should be on an individual basis, under unusual circumstances and at the discretion of the ICU director. These fall into two categories:

• Too well to benefit based on low risk. Examples given are patients after peripheral vascular surgery, hemodynamically stable diabetic ketoacidosis, mild congestive heart failure, conscious drug overdose

• Too sick to benefit based on condition consistent with imminent death. Examples given are patients with severe irreversible brain damage, irreversible multi-organ system failure, metastatic cancer unresponsive to therapy, patients with decisionmaking capability who decline services typically provided by ICUs, comfort care only.

Objective Parameters Model

Includes parameters of vital signs, laboratory values, radiological and other testing results that are consistent with severity of illness that may be helpful criteria for assessing usefulness and necessity of ICU services.

Discharge Criteria

ICU policies should stipulate objective criteria for determining when patients can be discharged from the ICU.

• Objective evidence of improvement or stabilization demonstrating no further benefit that could not be provided in a non-ICU stetting

• Objective evidence of deterioration and no further active intervention is planned

• Should be similar to the admitting criteria for the level of care to which the patient is being transferred

Triage Criteria

Often needed because the number of potential ICU patients exceeds the availablebeds

• May use the same prioritizing criteria listed under admission

• ICU/Critical Care Director should have the authority and responsibility to triage

• Triage decisions may be made without patient/surrogate consent

• Triage decisions may be made despite an anticipated untoward outcome

Summary of points potentially applicable to VALUE participants:

• ICUs should have protocols for admission, discharge and triage

• Criteria for admission, discharge and triage should be based on elements known to be influenced by ICU care. Some patients are too well to need ICU services, and some are too sick to benefit.

• The ICU/Critical Care Director has authority and responsibility over these protocols/criteria and their enforcement, and is therefore probably an important champion to recruit for this work.

• There are many severity/prognostic scoring tools, and ICU personnel should be familiar with them.

• None of the 3 models for determining ICU ‘appropriateness’ given in this guideline specifically use age as an element for guiding decisions

D. All About hemopneumothorax and pneumothorax

Pneumothorax

Background

A pneumothorax refers to a collection of gas in the pleural space resulting in collapse of the lung on the affected side. A tension pneumothorax is a life-threatening condition caused by air within the pleural space that is under pressure; displacing

mediastinal structures and compromising cardiopulmonary function. A traumatic pneumothorax results from blunt or penetrating injury that disrupts the parietal or visceral pleura. Mechanisms include injuries secondary to medical or surgical procedures

Pathophysiology

A tension pneumothorax results from any lung parenchymal or bronchial injury that acts as a one-way valve and allows free air to move into an intact pleural space but prevents the free exit of that air. In addition to this mechanism, the positive pressure used with mechanical ventilation therapy can cause air trapping.

As pressure within the intrapleural space increases, the heart and mediastinal structures are pushed to the contralateral side. The mediastinum impinges on and compresses the contralateral lung.

Hypoxia results as the collapsed lung on the affected side and the compressed lung on the contralateral side compromise effective gas exchange. This hypoxia and decreased venous return caused by compression of the relatively thin walls of the atria impair cardiac function. The decrease in cardiac output results in hypotension and, ultimately, in hemodynamic collapse and death to the patient, if untreated.

History

The signs and symptoms produced by tension pneumothorax are usually more impressive than those seen with a simple pneumothorax. Unlike the obvious patient presentations oftentimes used in medical training courses to describe a tension pneumothorax, actual case reports include descriptions of the diagnosis of the condition being missed or delayed because of subtle presentations that do not always present with the classically described clinical findings of this condition.

Symptoms and signs of tension pneumothorax may include the following:

Chest pain (90%), dyspnea (80%), anxiety, acute epigastric pain (a rare finding), fatigue

Physical

Findings at physical examination may include the following:

Respiratory distress (considered a universal finding) or respiratory arrest

Unilaterally decreased or absent lung sounds (a common finding; but decreased air entry may be absent even in an advanced state of the disease)

Adventitious lung sounds (crackles, wheeze; an ipsilateral finding)

Lung sounds transmitted from the nonaffected hemithorax are minimal with auscultation at the midaxillary line

Tachypnea; bradypnea (as a preterminal event)

Hyperresonance of the chest wall on percussion (a rare finding; may be absent even in an advanced state of the disease)

Hyperexpansion of the chest wall

Increasing resistance to providing adequate ventilation assistance

Cyanosis (a rare finding)

Tachycardia (a common finding)

Hypotension (should be considered as an inconsistently present finding; while hypotension is typically considered as a key sign of a tension pneumothorax, studies suggest that hypotension can be delayed until its appearance immediately precedes cardiovascular collapse)

Pulsus paradoxus

Jugular venous distension

Cardiac apical displacement (a rare finding)

Tracheal deviation (an inconsistent finding; while historic emphasis has been placed on tracheal deviation in the setting of tension pneumothorax, tracheal deviation is a relatively late finding caused by midline shift)

Mental status changes, including decreased alertness and/or consciousness (a rare finding)

Abdominal distension (from increased pressure in the thoracic cavity producing caudal deviation of the diaphragm and from secondary pneumoperitoneum produced as air dissects across the diaphragm through the pores of Kohn)

When examining a patient for suspected tension pneumothorax, helpful indications of subtle thoracic size and thoracic mobility differences may be elicited by performing careful visual inspection along the line of the thorax. In a supine patient, by lowering oneself to be in level with the patient.

Tension pneumothorax may be a difficult diagnosis to make and may present with considerable variability in signs presented. Respiratory distress and chest pain are generally accepted as being universally present in tension pneumothorax. Tachycardia and ipsilateral air entry are also common findings.

The development of tension pneumothorax in patients who are ventilated will generally be of faster onset with immediate, progressive arterial and mixed venous oxyhemoglobin saturation decline and immediate decline in cardiac output.

Cardiac arrest associated with asystole or pulseless electrical activity (PEA) may ultimately result.

Causes

A wide variety of disease states and circumstances increase the patient's risk of a pneumothorax. If a pneumothorax is complicated by a one-way valve effect, tension pneumothorax may result.

Infants requiring ventilatory assistance and those with meconium aspiration have a particularly high risk for tension pneumothorax. Aspirated meconium may serve as a one-way valve and produce a tension pneumothorax.

Trauma may cause a pneumothorax.

Tension pneumothorax may be the result of blunt trauma with or without associated rib fractures.

o Incidents that may cause tension pneumothoraces include unrestrained head-on motor vehicle accidents, falls, and altercations involving laterally directed blows.

o Any penetrating wound that produces an abnormal passageway for gas exchange into the pleural spaces and that results in air trapping may produce a tension pneumothorax.

o Significant chest injuries carry an estimated 10-50% risk of associated pneumothorax. In about half of these cases, the pneumothorax may be occult; therefore, chest CT should always be performed.

o In a recent study, 12% of patients with asymptomatic chest stab wounds had a delayed pneumothorax or hemothorax.

o McPherson et al, analyzing data from the Vietnam Wound Data and Munitions Effectiveness Team study, determined that tension pneumothorax the cause of death in 3-4% of fatally wounded combat casualties.2

Many procedures performed in an intensive care or emergency setting can result in an iatrogenic pneumothorax and tension pneumothorax. Examples of these procedures include incorrect chest tube insertion, mechanical ventilation therapy, central venous cannulation; cardiopulmonary resuscitation; hyperbaric oxygen therapy; needle, transbronchial, or transthoracic lung biopsy; liver biopsy or surgery; and neck surgery.

Secondary or spontaneous tension pneumothorax is possible in many medical conditions.

o Pneumothorax is associated with asthma, chronic obstructive pulmonary disease , pneumonia (especially with Staphylococcus, Klebsiella,

Pseudomonas, and Pneumocystis species), pertussis, tuberculosis, lung abscess, and cystic fibrosis.

o In pulmonary disorders such as asthma and emphysema, hyperexpansion disrupts the alveoli.

o Increased pulmonary pressure due to coughing with a bronchial plug of mucus or phlegm bronchial plug may play a role.

o Marfan syndrome is associated with an increased risk of pneumothorax.

o Individuals may inherit a predisposition for primary spontaneous pneumothorax.

o Although rare, spontaneous pneumothorax occurring bilaterally and progressing to tension pneumothorax has been documented.

Prehospital Care

Attention to the ABCs is mandatory for all patients with thoracic trauma. Evaluate the patency of the airway and the adequacy of the ventilatory effort. Assess the circulatory status and the integrity of the chest wall.

Failure of the emergency medical service personnel and medical control physician to make a correct diagnosis of tension pneumothorax and to promptly perform needle decompression in the prehospital setting can result in rapid clinical deterioration and cardiac arrest.

However, if an incorrect diagnosis of tension pneumothorax is made in the prehospital setting, the patient's life is endangered by unnecessary invasive procedures. Close cooperation and accurate communication between the emergency department and the emergency medical service personnel is of paramount importance.

To prevent reentry of air into the pleural cavity after needle thoracostomy and decompression in the prehospital setting, a one-way valve should be attached to the distal end of the Angiocath. If available, a Heimlich valve may be used. If a commercially prepared valve is not available, attach a finger condom or the finger of a rubber glove with its tip removed to serve as a makeshift one-way valve device.

Clothing covering a wound that communicates with the chest cavity can play a role in producing a one-way valve effect, allowing air to enter the pleural cavity but hindering its exit. Removing such clothing items from the wound may facilitate decompression of a tension pneumothorax.

A tension pneumothorax is a contraindication to the use of military antishock trousers.

In a preliminary 2006 study from Norway, Busch evaluated the feasibility of using portable ultrasound in an air rescue setting.5 Concluding that prehospital ultrasonography could provide diagnostic and therapeutic benefit when conducted by a proficient examiner who used goal-directed and time-sensitive protocols. Further study in this area may help to determine the indications and role of prehospital sonography.

Emergency Department Care

For all patients with thoracic injury, immediate and careful attention to the ABCs is vital. Fully assess the patency of the airway and adequacy of the ventilatory effort. Carefully evaluate the cardiovascular system because a tension pneumothorax and a pericardial tamponade can cause similar findings.

If a tension pneumothorax is suspected, immediately administer 100% oxygen, and evaluate the patient for evidence of respiratory compromise, hemodynamic

instability, or clinical deterioration. Place large-bore catheters, because hemothorax can be associated with pneumothorax, and the patient may, therefore, require immediate intravenous infusion. Upright positioning, if not inappropriate due to cervical spine or trauma concerns, may be beneficial.

Immediately perform needle thoracostomy or chest tube placement (see Procedures) if the clinical condition warrants such action. Once a needle thoracostomy has been performed, chest tube insertion must follow.

If a hemothorax is associated with the pneumothorax, additional chest tubes may be needed to assist drainage of blood and clots. If the hemopneumothorax requires insertion of a second chest tube, the second tube should be directed inferiorly and should be posterior to the diaphragm.

Chest tubes are attached to a vacuum apparatus that continually removes air from the pleural cavity. The collapsed lung reexpands and heals, thereby preventing continued air leakage. After air leaks have ceased for 24 hours, the vacuum may be decreased and the chest tube removed.

The process of lung reexpansion and healing is not immediate and may be complicated by pulmonary edema; therefore, a chest tube is usually left in place for at least 3 days unless the clinical condition warrants a longer placement.

In general, traumatic pneumothoraces should be treated with insertion of a chest tube, particularly if the patient cannot be closely observed.  

o A subset of patients who have a small (<15-20%), minimally symptomatic pneumothorax may be admitted, observed closely, and monitored by using serial chest radiographs.

o In these patients, administration of 100% oxygen promotes resolution by speeding the absorption of gas from the pleural cavity into the pulmonary vasculature.

Consultations

Treatment of tension pneumothorax should commence immediately after diagnosis, without waiting for further consultation and/or evaluation.

A trauma or general surgeon should evaluate patients with trauma, and the patient should be admitted for observation.

Medication

A tension pneumothorax requires treatment with procedural modalities. Anesthetics and analgesics should be used if the patient is not in distress. Medication may be necessary to treat the pulmonary disorder that caused the pneumothorax. For example, intravenous antibiotics are included in the treatment of a pneumothorax that developed as a sequela of staphylococcal pneumonia. Also, studies suggest that the administration of prophylactic antibiotics after chest tube insertion may reduce the incidence of complications such as emphysema.

Hemopneumothorax :

Introduction

Accumulation of blood within the chest, or hemothorax, is a relatively common problem, most often resulting from injury to intrathoracic structures or the chest wall. Hemothorax unrelated to trauma is considerably less common and can result from various causes. Prompt identification and treatment of traumatic hemothorax is an essential part of the care of the injured patient. In cases of hemothorax unrelated to trauma, a careful investigation for the underlying source must be performed while treatment is occurring

Etiology

By far, the most common cause of hemothorax is trauma. The various etiologies follow.

Traumatic o Blunt trauma

o Penetrating trauma (including iatrogenic)

Nontraumatic or spontaneous

o Neoplasia (primary or metastatic)

o Blood dyscrasias, including complications of anticoagulation

o Pulmonary embolism with infarction

o Torn pleural adhesions in association with spontaneous pneumothorax

o Bullous emphysema

o Necrotizing infections

o Tuberculosis  (Click here to complete a Medscape CME activity on screening for tuberculosis.)

o Pulmonary arteriovenous fistulae

o Hereditary hemorrhagic telangiectasia

o Nonpulmonary intrathoracic vascular pathology (eg, thoracic aortic aneurysm, aneurysm of the internal mammary artery)

o Intralobar and extralobar sequestration

o Abdominal pathology (eg, pancreatic pseudocyst, splenic artery aneurysm, hemoperitoneum)

o Catamenial

Pathophysiology

Bleeding into the pleural space can occur with virtually any disruption of the tissues of the chest wall and pleura or the intrathoracic structures.

The physiologic response to the development of a hemothorax is manifested in 2 major areas: hemodynamic and respiratory. The degree of hemodynamic response is determined by the amount and rapidity of blood loss.

Normal respiratory movement may be hampered by the space-occupying effect of a large accumulation of blood within the pleural space. In trauma cases, abnormalities of ventilation and oxygenation may result, especially if associated with injuries to the chest wall. In some cases of nontraumatic origin, especially those associated with pneumothorax and a limited amount of bleeding, respiratory symptoms may predominate.

Systemic physiologic response - Hemodynamic

Hemodynamic changes vary depending on the amount of bleeding and the rapidity of blood loss. Blood loss of up to 750 mL in a 70-kg man should cause no significant hemodynamic change. Loss of 750-1500 mL in the same individual will cause the early symptoms of shock, ie, tachycardia, tachypnea, and a decrease in pulse pressure.

Significant signs of shock with signs of poor perfusion occur with loss of blood volume of 30% or more (1500-2000 mL). Because the pleural cavity of a 70-kg man can hold 4 or more liters of blood, exsanguinating hemorrhage can occur without external evidence of blood loss.

Systemic physiologic response - Respiratory

Blood occupying the pleural cavity takes up space that the lung would fill in normal respiratory excursion. A large enough collection causes the patient to complain of dyspnea and may produce the clinical finding of tachypnea. The volume of blood required to produce these symptoms in a given individual varies depending on a number of factors, including organs injured, severity of injury, and underlying pulmonary and cardiac reserve.

Dyspnea is a common symptom in cases in which hemothorax develops in an insidious manner, such as those secondary to metastatic disease. Blood loss in such cases is not acute as to produce a visible hemodynamic response, and dyspnea is often the predominant complaint.

Physiologic resolution of the hemothorax

Blood that enters the pleural cavity is exposed to the motion of the diaphragm, lungs, and other intrathoracic structures. This results in some degree of defibrination of the blood so that incomplete clotting occurs. Within several hours of cessation of bleeding, lysis of existing clots by pleural enzymes begins.

Lysis of red blood cells results in a marked increase in the protein concentration of the pleural fluid and an increase in the osmotic pressure within the pleural cavity. This elevated intrapleural osmotic pressure produces an osmotic gradient between the pleural space and the surrounding tissues that favors transudation of fluid into the pleural space. In this way, a small and

asymptomatic hemothorax can progress into a large and symptomatic bloody pleural effusion.

Late physiologic sequelae of unresolved hemothorax

Two pathologic states are associated with the later stages of hemothorax. These include empyema and fibrothorax.

Empyema results from bacterial contamination of the retained hemothorax. If undetected or improperly treated, this can lead to bacteremia and septic shock.

Fibrothorax results when fibrin deposition develops in an organized hemothorax and coats both the parietal and visceral pleural surfaces, trapping the lung. The lung is fixed in position by this adhesive process and is unable to fully expand. Persistent atelectasis of portions of the lung and reduced pulmonary function result from this process.

Traumatic hemothorax

Symptoms and physical findings associated with hemothorax in trauma vary widely depending on the amount and rapidity of bleeding, the existence and severity of underlying pulmonary disease, the nature and degree of associated injuries, and the mechanism of injury.

Blunt trauma - Hemothorax with blunt chest wall injuries o Hemothorax is rarely a solitary finding in blunt trauma. Associated

chest wall or pulmonary injuries are nearly always present.

o Simple bony injuries consisting of one or multiple rib fractures are the most common blunt chest injuries. A small hemothorax may be associated with even single rib fractures but often remains unnoticed during the physical examination and even after chest radiography. Such small collections rarely need treatment.

o Complex chest wall injuries are those in which either 4 or more sequential single rib fractures are present or a flail chest exists. These types of injuries are associated with a significant degree of chest wall damage and often produce large collections of blood within the pleural cavity and substantial respiratory impairment. Pulmonary contusion and pneumothorax are commonly associated injuries. Injuries resulting in laceration of intercostal or internal mammary arteries may produce a hemothorax of significant size and significant hemodynamic compromise. These vessels are the most common source of persistent bleeding from the chest after trauma.

o Delayed hemothorax can occur at some interval after blunt chest trauma. In such cases, the initial evaluation, including chest radiography, reveals findings of rib fractures without any accompanying intrathoracic pathology. However, hours to days later, a hemothorax is seen. The mechanism is believed to be either rupture of a trauma-associated chest wall hematoma into the pleural space or

displacement of rib fracture edges with eventual disruption of intercostal vessels during respiratory movement or coughing.

Blunt intrathoracic injuries

o Large hemothoraces are usually related to injury of vascular structures. Disruption or laceration of major arterial or venous structures within the chest may result in massive or exsanguinating hemorrhage.

o Hemodynamic manifestations associated with massive hemothorax are those of hemorrhagic shock. Symptoms can range from mild to profound, depending on the amount and rate of bleeding into the chest cavity and the nature and severity of associated injuries.

o Because a large collection of blood will compress the ipsilateral lung, related respiratory manifestations include tachypnea and, in some cases, hypoxemia.

o A variety of physical findings such as bruising, pain, instability or crepitus upon palpation over fractured ribs, chest wall deformity, or paradoxical chest wall movement may lead to the possibility of coexisting hemothorax in cases of blunt chest wall injury. Dullness to percussion over a portion of the affected hemithorax is often noted and is more commonly found over the more dependent areas of the thorax if the patient is upright. Decreased or absent breath sounds upon auscultation are noted over the area of hemothorax.

Penetrating trauma

o Hemothorax from penetrating injury is most commonly caused by direct laceration of a blood vessel. While arteries of the chest wall are most commonly the source of hemothorax in penetrating injury, intrathoracic structures, including the heart, should also be considered.

o Pulmonary parenchymal injury is very common in cases of penetrating injury and usually results in a combination of hemothorax and pneumothorax. Bleeding in these cases is usually self-limited.

Nontraumatic hemothorax

Symptoms and physical findings are variable, depending on the underlying pathology.

Hemothorax secondary to acute hemorrhage from structures within the chest can produce profound hemodynamic changes and symptoms of shock. Massive hemothorax can result from vascular structures such as a ruptured or leaking thoracic aortic aneurysm or from pulmonary sources such as lobar sequestration or arteriovenous malformation. Disruption of a vascular pleural adhesion unrelated to trauma can produce a significant hemothorax with an associated spontaneous pneumothorax.

Occult hemorrhage is most commonly related to metastatic disease or complications of anticoagulation. In these situations, bleeding into the pleural

cavity occurs slowly, resulting in subtle or absent changes in hemodynamics. When the effusion is large enough to produce symptoms, dyspnea is usually the most prominent complaint. Signs of anemia may also be present. Physical examination reveals findings similar to those for any pleural effusion, with dullness to percussion and decreased breath sounds noted over the area of the effusion.

Hemothorax in conjunction with pulmonary infarction is usually preceded by clinical findings associated with pulmonary embolism.

Catamenial hemothorax is an unusual problem related to thoracic endometriosis. Hemorrhage into the thorax is periodic, coinciding with the patient's menstrual cycle.

Indications

If a hemothorax is equal to or greater than the amount required to obscure the costophrenic sulcus or is found in association with a pneumothorax based on chest radiograph findings, it should be drained by tube thoracostomy. In cases of hemopneumothorax, 2 chest tubes may be preferred, with the tube draining the pneumothorax placed in a more superior and anterior position.

Surgical exploration in cases of traumatic hemothorax should be performed in the following circumstances:

Greater than 1000 mL of blood is evacuated immediately after tube thoracostomy. This is considered a massive hemothorax.

Bleeding from the chest continues, defined as 150-200 mL/h for 2-4 hours.

Persistent blood transfusion is required to maintain hemodynamic stability.

The late sequelae of hemothorax, including residual clot, infected collections, and trapped lung, require additional treatment and, most often, surgical intervention.

Retained clot (defined as an undrained collection of 500 mL or more as estimated by CT scan findings or opacification of one third or more of the chest on chest radiographs) is a well-known sequela after initial tube thoracostomy for hemothorax and should be evacuated early in the patient's hospital course, if the clinical condition permits. Early intervention in the case of a retained clot can be performed with thoracoscopy, provided the operation is planned within 1 week of the bleeding episode.

Empyema usually develops from superimposed infection in a retained collection of blood. It requires surgical drainage and, possibly, decortication.

Fibrothorax is a late uncommon complication that can result from retained hemothorax. Thoracotomy and decortication are required for treatment.

Relevant Anatomy

Extrapleural

In cases of trauma, disruption of the chest wall tissues with violation of the pleural membrane can cause bleeding into the pleural cavity. The most likely sources of significant or persistent bleeding from chest wall injuries are the intercostal and internal mammary arteries.

In nontraumatic cases, rare disease processes within the chest wall (eg, bony exostoses) can be responsible.

Intrapleural

Blunt or penetrating injury involving virtually any intrathoracic structure can result in hemothorax. Massive hemothorax or exsanguinating hemorrhage may result from injury to major arterial or venous structures contained within the thorax or from the heart itself. These include the aorta and its brachiocephalic branches, the main or branch pulmonary arteries, the superior vena cava and the brachiocephalic veins, the inferior vena cava, the azygous vein, and the major pulmonary veins.

Injury to the heart can produce a hemothorax if a communication exists between the pericardium and the pleural space.

Injury to the pulmonary parenchyma may cause hemothorax, but it is usually self-limited because pulmonary vascular pressure is normally low. Pulmonary parenchymal injury is usually associated with pneumothorax and results in limited hemorrhage.

Hemothorax resulting from metastatic malignant disease is usually from tumor implants that seed the pleural surfaces of the thorax.

Diseases of the thoracic aorta and its major branches, such as dissection or aneurysm formation, account for a large percentage of specific vascular abnormalities that can cause hemothorax. Aneurysms of other intrathoracic arteries such as the internal mammary artery have been described and are possible causes of hemothorax if rupture occurs.

A variety of unusual congenital pulmonary abnormalities, including intra- and extralobar sequestration, hereditary telangiectasia, and congenital arteriovenous malformations, can cause hemothorax.

Hemothorax can result from pathology originating within the abdomen if bleeding from the abnormality is able to traverse the diaphragm through one of the normal hiatal openings or a congenital or acquired opening.

Contraindications

Needle aspiration of a hemothorax is generally not indicated for definitive treatment.

In some cases of nontraumatic hemothorax, especially those that occur from metastatic pleural implants, patients may present with the finding of a new pleural effusion of unknown etiology and hemothorax may not be identified until the initial diagnostic aspiration is performed. Although the diagnostic evaluation in such cases may be performed using needle aspiration, complete evacuation of these collections

often requires treatment with tube thoracostomy, similar to hemothoraces resulting from other causes.

Although not contraindicated, drainage of hemothorax or any pleural effusion in an individual with a coagulopathy should be performed with great care. This group includes patients receiving anticoagulation therapy and those with significant liver disease or inherited coagulation factor deficiencies. Normalization of coagulation function by cessation of anticoagulants and/or correction of factor deficiencies using appropriate blood products, if necessary, should be initiated prior to a drainage procedure, if possible.

Needle aspiration should not be performed if clotting deficiencies are present. Rather, tube thoracostomy should be used, with the ability to visualize and control any chest wall bleeding that is encountered. If necessary, in individuals requiring long-term anticoagulant therapy, this medication can be resumed 8-12 hours after the thoracostomy has been completed.

Tube thoracostomy drainage of a hemothorax is relatively contraindicated when significant pleural adhesions are known to be present. Incomplete drainage or inability to effectively access the area is likely. Also, blunt division of pleural adhesions may cause additional bleeding and result in lung laceration. If evacuation of such collections is mandated clinically, thoracotomy with division of adhesions under direct vision is the safer approach.

Medical Therapy

Intrapleural instillation of fibrinolytic agents is advocated in some centers for evacuation of residual hemothorax in cases in which initial tube thoracostomy drainage is inadequate. The proposed dose is 250,000 IU of streptokinase or 100,000 IU of urokinase in 100 mL of sterile saline.5

Ventilator management should progress according to the individual status of the patient. In cases in which no other significant injury or disease process is present, weaning and extubation may proceed in a routine fashion. In more critically ill patients such as those with severe chest wall injuries or those requiring massive transfusion, ventilator management must be tailored to the condition of the patient.

After extubation, pulmonary toilet and adequate pain control are critical in preventing pulmonary complications such as atelectasis and pneumonia.

Chest tubes are maintained on underwater seal suction, and the volume of drainage and air leak are noted and recorded daily. If pulmonary injury is found or resection of lung tissue is required at the time of surgery, chest tubes are not removed until any air leak has disappeared and the lung is observed to be fully expanded on the chest x-ray film. Drainage should be less than 100 mL in 24 hours before chest tube removal.

Antibiotic coverage begun prior to surgery should be discontinued after 48 hours unless a definite reason exists for continuance.

Surgical Therapy

Tube thoracostomy drainage

Tube thoracostomy drainage is the primary mode of treatment for hemothorax. In adult patients, large-bore chest tubes, usually 36-42F, should be used to achieve adequate drainage in adults. Smaller-caliber tubes are more likely to occlude. In pediatric patients, chest tube size varies with the size of the child. In patients older than 12 years, the chest tube size used is usually the same as that for adults. In smaller children, a 24-34F chest tube should be used, depending on the size of the child.

Thoracostomy tube placement for hemothorax should ideally be in the sixth or seventh intercostal space at the posterior axillary line. In the supine trauma victim, a common error in chest tube insertion is placement too anteriorly and superiorly, making complete drainage very unlikely.

After tube thoracostomy is performed, a repeat chest radiograph should always be obtained. This helps identify chest tube position, helps determine completeness of the hemothorax evacuation, and may reveal other intrathoracic pathology previously obscured by the hemothorax. If drainage is incomplete as visualized on the postthoracostomy chest radiograph, placement of a second drainage tube should be considered. Preferably, a video-assisted thoracic surgery (VATS) operative procedure should be undertaken to evacuate the pleural space.

Some controversy exists regarding the management of retained clot after tube thoracostomy. Opinions range from conservative watchfulness to additional chest tube placement to surgical evacuation. Current opinion seems to favor some form of clot evacuation. Many trauma centers are moving away from additional tube thoracostomy and, instead, advocating an early VATS procedure. This is usually performed within 7-8 days of the initial injury and, in some centers, is performed within 48-72 hours if a retained clot is identified within the thorax.

Surgical exploration of the chest

Thoracotomy is the procedure of choice for surgical exploration of the chest when massive hemothorax or persistent bleeding is present. At the time of surgical exploration, the source of bleeding is controlled and the hemothorax is evacuated.

Surgical exploration of hemothorax may be performed using VATS in selected cases. Several centers have used this modality successfully to help identify and control the source of bleeding in a number of cases.

VATS evacuation of the hemothorax or retained clot can be performed safely. One-lung ventilation is not required. A single lumen tube can be used with directions to the anesthesiologist to decrease tidal volume or intermittently hold ventilation during the procedure. If cardiac, great vessel, or tracheobronchial injury is found, conversion to thoracotomy can be performed expeditiously.

Surgical exploration of the chest may be required later in the course of the patient with hemothorax for evacuation of retained clot, drainage of empyema, and/or decortication. Cases with retained clot can often be treated successfully with a VATS procedure, especially if this is accomplished within 7 days of initial drainage of the hemothorax. Thoracotomy is usually required for adequate empyema drainage or decortication.

In nontraumatic cases of hemothorax resulting from surgically correctable intrathoracic pathology, correction of the underlying disease process and evacuation of the hemothorax should be undertaken. This may include stapling and/or resection of bullous disease, resection of cavitary disease, resection of necrotic lung tissue, sequestration of arteriovenous malformations, or resection and/or repair of vascular abnormalities such as aortic aneurysms

E. Bioethics Aspects in Emergency

Doctrine of Informed Consent:

Under the modern doctrine of informed consent, a physician should discuss with the patient the following elements; the patient’s diagnosis, the nature and purpose of the proposed treatment, the risks and expected outcomes of the proposed treatment, alternative treatments and their risks, and the consequences of no treatment.

In order to successfully sue for lack of informed consent, a plaintiff must prove that 1) the physician failed to obtain full and informed consent and 2) this failure proximately caused the injury, that is, that the patient would not have consented to the procedure had the material risks been disclosed. Regarding the first element, most juridiscations follow a physician – oriented standard of disclosure. Under this standard, a physician is required to disclosure what a reasonable medical practitioner of the same school in the same or similar circumstances would disclose. However, a number of jurisdictions, including New Jersey and Pennsylvania, follow a patient – oriented standard disclosure. Under this standard, a physician is required to disclose the information that a reasonable persom in the patient’s situation would consider important in choosing a course of treatment. Reasonable people can disagree about which standard is more appropriate. The physician-oriented standard. The physician-oriented standard is sometimes deribed as allowing the medical community to specify its own scope of disclosure, which may be out of touch with the needs of the individual patient. By contrast, detractors of the patient-oriented standard point out that it is too prone to misuse by sympathetic juries in case where inevitable the undisclosed, unusual complication has occurred.

In order to prove the causation element, most jurisdictions require that plaintiff prove that a reasonable person in the patient’s situation would not have consented to the proposed treatment had adequate information been given.

Exception to consent requirements :

Several exeptions to informed-consent-disclosure requirements have been consistently recognized throughout the United States. In medical emergencies, when the patient is unconscious or unable to communicate, or when there is no time to obtain informed consent, the physician may provide treatment under the theory of implied consent. In this circumstance, the law presumes that the compelling need for treatment outweighs the need to obtain informed consent. When a patient receives recurrent medical care and thus has prior knowledge of the nature of the ongoing treatment, as well as the material risks and alternatives, then the physician generally need not make duplicative disclosures in order to obtain informed consent. However, if the patient’s condition or other circumstances change, the physician should appraise the patient of this change and renew the consent previously obtained.

A patient may expressly waive it right to informed consent by stating that he or she does not wish to be informed about certain information pertaining to the caourse of treatment. When this occurs, the physician should inquire why the patient does not wish to be informed and should document these reasons in the medical record. If the patient knowingly and intelligently waives this right, and has reasonable justifications for doing so, then nondisclosure will be defensible in court.

The final exception to consent requirements is known as the doctrine of therapeutic privilege. It arises in situations in which the patient is so anxious or fragile that full disclosure might cause serious emotional or physical harm. Circumstances justifying use of this doctrine are exceptionally rare, and physicians asserting this privillage must carefully document their decision making in the medical record. A physician’s concern that the patient might forego recommended treatment if adequately apprised of it risks is not a sufficient reason to invoke this doctrine

COMMENTS:

1) Inform Refusal must be obtained by patients or guardians who refuses to

undergo a certain medical procedure or treatmeant.

2) Doing the WSD procedure is not included in the General Practioner (GP).

3) Hypovolemic shock is noted in circulation deficiency, so adequate fluid

resuscitation is required for the vitals to improve.

4) We need to determine the severity of blood loss in hemorrhagic patients.

5) Selection of fluids need to be used wisely during fluid resuscitation.

6) In handling patients who undergo shock, primary survey (ABCDE) and

secondary survey must be done in a good manner.

7) All traumatic patient need to be treated under the hypovolemic shock

management. After that, we treat the underlying causes.

CONCLUSION:

In conclusion, 60 years old man who came to the Emergency Department is

having femur fracture and hemopneumothorax which causes hypovolemic shock. The

refusal from the patient’s family members about the WSD procedure must be

documented in the inform refusal

REFERENCE:

1) William F. Young, Jr., MD . Shock. C. Keith Stone, Roger L. Humphries.

Current Diagnosis & Treatment Emergency Medicine. 6th Edition. USA.

McGraw Hill Lange. 2008. 160 – 166.

2) Charles A Eckerline, Jr., MD, FACEP, Steven D. Rothert, MD, Jr. Legal

Aspects of Emergency Cases. C. Keith Stone, Roger L. Humphries. Current

Diagnosis & Treatment Emergency Medicine. 6th Edition. USA. McGraw Hill

Lange. 2008. 46 – 57

3) William Randall Partin, MD. Emergency Procedures. C. Keith Stone, Roger L.

Humphries. Current Diagnosis & Treatment Emergency Medicine. 6th Edition.

USA. McGraw Hill Lange. 2008. 58 – 125

4) Guyton & Hall, textbook Of Medical Physiology, Eleventh Edition, Elsevier,

2006: 823-824.

5) Nicholas A. Boon, Nicki R. Colledge, Brian R. Walker, Davision’s Principles

& Practice Of Medicine, 20th Edition, Churchill Livingstone Elsevier, 2006:

856.