In Partial Fulfillment of the Related Experience At Veterans Memorial Medical Center Diliman, Quezon city

Case Study of Septic Shock

Sumbitted by: Ariola, Irene mae V. Diongson Rolando V.

Submitted to: Sir Dave Tandoc RN,MAN Date Submitted: March 8, 2013

Introduction:
Septic shock is a life-threatening condition that happens when your blood pressure drops to a dangerously low level. The fall in blood pressure is a reaction to a serious infection that develops in the blood. This causes a response from the body known as sepsis. If sepsis is not treated, it will lead to septic shock. Symptoms of septic Shock includes cold skin and an increased heartbeat. If you have septic shock, you will usually be admitted to an intensive care unit (ICU) so that your bodys functions and organs can be supported while the infection is treated.

Symptoms:
Septic shock can affect any part of the body, including the heart, brain, kidneys, liver, and intestines. Symptoms may include: Cool, pale extremities High or very low temperature, chills Lightheadedness Low blood pressure, especially when standing Palpitations Rapid heart rate Restlessness, agitation, lethargy, or confusion Shortness of breath Skin rash or discoloration

elderly people Anyone who is taking immunosuppressive medications (such as transplant recipients) People who are being treated with chemotherapy drugs or radiation People who have had their spleen surgically removed (the spleen helps fight certain infections) People taking steroids (especially over the long term) People with longstanding diabetes, AIDS, or cirrhosis Someone who has very large burns or severe injuries People with infections such as o pneumonia,

o o o

meningitis, cellulitis, urinary tract infection

Risk factors for septic shock include:

Diabetes Diseases of the genitourinary system, biliary system, or intestinal system Diseases that weaken the immune system such as AIDS Indwelling catheters (those that remain in place for extended periods, especially intravenous lines and urinary catheters and plastic and metal stents used for drainage) Leukemia Long-term use of antibiotics Lymphoma Recent infection Recent surgery or medical procedure Recent use of steroid medications

Sepsis
Sepsis occurs when an infection spreads through the blood, causing symptoms to develop throughout the whole body. The term sepsis is sometimes used to refer to blood poisoning (septicaemia). This is not entirely accurate because sepsis is not just limited to the blood but affects the whole body, including the organs. Sepsis is usually caused by a bacterial infection, but it can sometimes be caused by viral or fungal infections.

The effects of sepsis:

Sepsis can affect many of the vital processes of the body including: blood pressure

breathing organ function Sepsis can result in septic shock if it is not treated immediately.

Classification of shock:
Shock is identified in most patients by hypotension and inadequate organ perfusion, which may be caused by either low cardiac output or low systemic vascular resistance. Circulatory shock can be subdivided into 4 distinct classes on the basis of underlying mechanism and characteristic hemodynamics, as follows:

Hypovolemic shock Obstructive shock Distributive shock Cardiogenic shock These classes of shock should be considered and systemically differentiated before establishing a definitive diagnosis of septic shock. Hypovolemic shock results from the loss of blood volume caused by such conditions as gastrointestinal (GI) bleeding, extravasation of plasma, major surgery, trauma, and severe burns. The patient demonstrates tachycardia, cool clammy extremities, hypotension, dry skin and mucus membranes, and poor turgor. Obstructive shock results from impedance of circulation by an intrinsic or extrinsic obstruction. Pulmonary embolism and pericardial tamponade both result in obstructive shock. Distributive shock is caused by such conditions as direct arteriovenous shunting and is characterized by decreased resistance or increased venous capacity from the vasomotor dysfunction. These patients have high cardiac output, hypotension, large pulse pressure, a low diastolic pressure, and warm extremities with a good capillary refill. These findings on physical examination strongly suggest a working diagnosis of septic shock. Cardiogenic shock is characterized by primary myocardial dysfunction, resulting in the inability of the heart to maintain adequate cardiac output. These patients demonstrate clinical signs of low cardiac output, while evidence exists of adequate intravascular volume. The patients have cool clammy extremities, poor capillary refill, tachycardia, narrow pulse pressure, and a low urine output.

Anatomy and Physiology:

The respiratory system is situated in the thorax, and is responsible for gaseous exchange between the circulatory system and the outside world. Air is taken in via the upper airways (the nasal cavity, pharynx and larynx) through the lower airways (trachea, primary bronchi and bronchial tree) and into the small bronchioles and alveoli within the lung tissue. The lungs are divided into lobes; The left lung is composed of the upper lobe, the lower lobe and the lingula (a small remnant next to the apex of the heart), the right lung is composed of the upper, the middle and the lower lobes. The Nose The uppermost portion of the human respiratory system, the nose is a hollow air passage that functions in breathing and in the sense of smell. The nasal cavity moistens and warms incoming air, while small hairs and mucus filter out harmful particles and microorganisms. This illustration depicts the interior of the human nose. The prominent structure between the eyes that serves as the entrance to the respiratory tract and contains the olfactory organ. It provides air for respiration, serves the sense of smell, conditions the air by filtering, warming, and moistening it, and cleans itself of foreign debris extracted from inhalations. The Trachea, Bronchi Aviolar Ducts and Avioli: The trachea (windpipe) divides into two main bronchi (also mainstem bronchi), the left and the right, at the level of the sternal angle at the anatomical point known as the carina. The right main bronchus is wider, shorter, and more vertical than the left main bronchus. The right main bronchus subdivides into three lobar bronchi while the left main bronchus divides into two. The lobar bronchi divide into tertiary bronchi, also known as segmental bronchi, each of which supplies a bronchopulmonary segment. A bronchopulmonary segment is a division of a lung that is separated from the rest of the lung by a connective tissue septum.. This property allows a bronchopulmonary segment to be surgically removed

without affecting other segments. There are ten segments per lung, but due to anatomic development, several segmental bronchi in the left lung fuse, giving rise to eight. The segmental bronchi divide into many primary bronchioles which divide into terminal bronchioles, each of which then gives rise to several respiratory bronchioles, which go on to divide into 2 to 11 alveolar ducts. There are 5 or 6 alveolar sacs associated with each alveolar duct. The alveolus is the basic anatomical unit of gas exchange in the lung. There is hyaline cartilage present in the bronchi, present as irregular rings in the larger bronchi (and not as regular as in the trachea), and as small plates and islands in the smaller bronchi. Smooth muscle is present continuously around the bronchi. In the mediastinum, at the level of the fifth thoracic vertebra, the trachea divides into the right and left primary bronchi. The bronchi branch into smaller and smaller passageways until they terminate in tiny air sacs called alveoli. The cartilage and mucous membrane of the primary bronchi are similar to that in the trachea. As the branching continues through the bronchial tree, the amount of hyaline cartilage in the walls decreases until it is absent in the smallest bronchioles. As the cartilage decreases, the amount of smooth muscle increases. The mucous membrane also undergoes a transition from ciliated pseudostratified columnar epithelium to simple cuboidal epithelium to simple squamous epithelium. The alveolar ducts and alveoli consist primarily of simple squamous epithelium, which permits rapid diffusion of oxygen and carbon dioxide. Exchange of gases between the air in the lungs and the blood in the capillaries occurs across the walls of the alveolar ducts and alveoli. The Lungs: The lungs constitute the largest organ in the respiratory system. They play an important role in respiration, or the process of providing the body with oxygen and releasing carbon dioxide. The lungs expand and contract up to

20 times per minute taking in and disposing of those gases. Air that is breathed in is filled with oxygen and goes to the trachea, which branches off into one of two bronchi. Each bronchus enters a lung. There are two lungs, one on each side of the breastbone and protected by the ribs. Each lung is made up of lobes, or sections. There are three lobes in the right lung and two lobes in the left one. The lungs are cone shaped and made of elastic, spongy tissue. Within the lungs, the bronchi branch out into minute pathways that go through the lung tissue. The pathways are called bronchioles, and they end at microscopic air sacs called alveoli. The alveoli are surrounded by capillaries and provide oxygen for the blood in these vessels. The oxygenated blood is then pumped by the heart throughout the body. The alveoli also take in carbon dioxide, which is then exhaled from the body. Inhaling is due to contractions of the diaphragm and of muscles between the ribs. Exhaling results from relaxation of those muscles. Each lung is surrounded by a two-layered membrane, or the pleura, that under normal circumstances has a very, very small amount of fluid between the layers. The fluid allows the membranes to easily slide over each other during breathing. Mechanics of Breathing: To take a breath in, the external intercostal muscles contract, moving the ribcage up and out. The diaphragm moves down at the same time, creating negative pressure within the thorax. The lungs are held to the thoracic wall by the pleural membranes, and so expand outwards as well. This creates negative pressure within the lungs, and so air rushes in through the upper and lower airways. Expiration is mainly due to the natural elasticity of the lungs, which tend to collapse if they are not held against the thoracic wall. This is the mechanism behind lung collapse if there is air in the pleural space (pneumothorax). Physiology of Gas Exchange: Each branch of the bronchial tree eventually sub-divides to form very narrow terminal bronchioles, which terminate in the alveoli. There are many millions of alveoli in each lung, and these are the areas responsible for

gaseous exchange, presenting a massive surface area for exchange to occur over. Each alveolus is very closely associated with a network of capillaries containing deoxygenated blood from the pulmonary artery. The capillary and alveolar walls are very thin, allowing rapid exchange of gases by passive diffusion along concentration gradients. CO2 moves into the alveolus as the concentration is much lower in the alveolus than in the blood, and O2 moves out of the alveolus as the continuous flow of blood through the capillaries prevents saturation of the blood with O2 and allows maximal transfer across the membrane.

Pathophysiology:
The pathophysiology of septic shock is not precisely understood, but it involves a complex interaction between the pathogen and the hosts immune system. The normal physiologic response to localized infection includes the activation of host defense mechanisms that result in the influx of activated neutrophils and monocytes, the release of inflammatory mediators, local vasodilation, increased endothelial permeability, and activation of coagulation pathways. These mechanisms are in play during septic shock, but on a systemic scale, leading to diffuse endothelial disruption, vascular permeability, vasodilation, and thrombosis of end-organ capillaries. Endothelial damage itself can further activate inflammatory and coagulation cascades, creating in effect a positive feedback loop, and leading to further endothelial and end-organ damage. Endotoxinstimulation of humoral and cellular immune systemsactivation of complement sequence and coagulation cascade Activation of coagulation cascade activation of fibrinolytic system DIC Complement activationchemotaxis of PMNs, degranulation of mast cells, and release of histamine and inflammatory mediatorsincreased capillary permeability INFLAMMATION release of catecholamines and prostaglandins generalized vasoconstriction VASOCONSTRICTION decreased perfusion of vital organs tissue hypoxia metabolic acidosis METABOLIC ACIDOSIS capillary pooling decreased circulating blood volume decreased venous return decreased cardiac output DECREASED CARDIAC OUTPUT decreased coronary and cerebral blood flow intractable hypotension, coma, multiorgan failure DEATH

Exams and Tests:

Blood tests may be done to check for infection, low blood oxygen level, disturbances in the body's acid-base balance, or poor organ function or organ failure. A chest x-ray may show pneumonia or fluid in the lungs (pulmonary edema). A urine sample may show infection. Additional studies, such as blood cultures, may not become positive for several days after the blood has been taken, or for several days after the shock has developed.

Treatment:
Septic shock is a medical emergency. Patients are usually admitted to the intensive care unit of the hospital. Treatment may include:

Breathing machine (mechanical ventilation) Drugs to treat low blood pressure, infection, or blood clotting Fluids given directly into a vein (intravenously) Oxygen Surgery There are new drugs that act against the extreme inflammatory response seen in septic shock. These may help limit organ damage. Hemodynamic monitoring -- the evaluation of the pressures in the heart and lungs -- may be required. This can only be done with special equipment and intensive care nursing

EARLY MANAGEMENT The first priority in any patient with severe sepsis or septic shock is stabilization of their airway and breathing. Next, perfusion to the peripheral tissues should be restored.

Stabilize respiration
Supplemental oxygen should be supplied to all patients with sepsis and oxygenation should be monitored continuously with pulse oximetry. Intubation and mechanical ventilation may be required to support the increased work of breathing that typically accompanies sepsis, or for airway protection since encephalopathy and a depressed level of consciousness frequently complicate sepsis. Sedative and induction agents (eg, etomidate) used to intubate patients with severe sepsis or septic shock are discussed separately. Other aspects of intubation and mechanical ventilation are similarly described elsewhere. (See "Sedation or induction agents for rapid sequence intubation in adults" and"Advanced emergency airway management in adults" and "Rapid sequence intubation in adults" and"The decision to intubate" and "The difficult airway in adults".) Chest radiographs and arterial blood analysis should be obtained following initial stabilization. These studies are used in combination with other clinical parameters to diagnose acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), which frequently complicate sepsis. (See "Acute respiratory distress syndrome: Clinical features and diagnosis" and "Mechanical ventilation in acute respiratory distress syndrome".)

Assess perfusion
Once the patient's respiratory status has been stabilized, the adequacy of perfusion should be assessed. Hypotension is the most common indicator that perfusion is inadequate. Therefore, it is important that the blood pressure be assessed early and often. An arterial catheter may be inserted if blood pressure is labile or restoration of arterial perfusion pressures is expected to be a protracted process, because a sphygmomanometer may be unreliable in hypotensive patients [8]. Attempts to insert an arterial line

should not be allowed to delay the prompt management of shock. (See "Arterial catheterization techniques for invasive monitoring".) Critical hypoperfusion can also occur in the absence of hypotension, especially during early sepsis. Thus, clinical evidence of impaired perfusion should be sought in all patients with sepsis. Common signs of hypoperfusion include cool, vasoconstricted skin due to redirection of blood flow to core organs (although warm, flushed skin may be present in the early phases of sepsis), obtundation or restlessness, oliguria or anuria, and lactic acidosis. These findings may be modified by preexisting disease or medications. As an example, elderly patients, diabetic patients, and patients who take beta-blockers may not exhibit an appropriate tachycardia as blood pressure falls. Patients with chronic hypertension may develop critical hypoperfusion at a higher blood pressure than healthy patients (ie, relative hypotension).

Catheters
After initial assessment, a central venous catheter (CVC) should be inserted in most patients with severe sepsis or septic shock. A CVC can be used to infuse intravenous fluids, infuse medications, infuse blood products, and draw blood. In addition, it can be used for hemodynamic monitoring by measuring the central venous pressure (CVP) and the central venous oxyhemoglobin saturation (ScvO2). In one clinical trial, treatment of septic shock guided by the ScvO2 reduced mortality

Ongoing management
There are two possible outcomes following the interventions described above:

Despite aggressive therapy, the patient may have persistent hypoperfusion and progressive organ failure. This should prompt reassessment of the adequacy of the above therapies, antimicrobial regimen, and control of the septic focus, as well as the accuracy of the diagnosis and the possibility that unexpected complications or coexisting problems have intervened (eg, pneumothorax following CVC insertion). The patient may have responded to the above interventions with restored perfusion and a ScvO2 greater than 70 percent. Such patients should continue to have their clinical and laboratory parameters followed closely. These include blood pressure, arterial lactate, urine output, creatinine, platelet count, Glasgow coma scale score, serum bilirubin, liver enzymes, oxygenation (ie, arterial oxygen tension or oxyhemoglobin saturation), and gut function (table 4). Reevaluation is indicated if any of these parameters worsen or fail to improve.

In early sepsis, most lactate is probably a byproduct of anaerobic metabolism due to organ hypoperfusion. Supporting this view, early goaldirected therapy decreases lactate levels faster than conventional therapy After the restoration of perfusion, however, lactate is probably due to causes other than anaerobic metabolism and further increasing oxygen delivery to the peripheral tissues is unlikely to decrease its levels . As a result, lactate values are generally unhelpful following restoration of perfusion, with one exception a rising lactate level should prompt reevaluation of perfusion (see "Venous blood gases and other alternatives to arterial blood gases"

Patients Profile:

Name:Arsenio Nacino Address:7704 Coronado St. Guadalupe Viejo Makati City Birthday:May 25, 1917 Age: 96 years old Gender:Male Citizenship:Filipino Religion:Roman Catholic Attending Physician: Arnold DG. Germar, MD Date Admitted: February 23, 2013 Time:5:45 pm Diagnosis: Septic Shock secondary to Acute Respiratory Failure secondary to Community Acquired Pneumonia

Interval History: Patient is a known hypertensive non February19,2013 managed as acase of CAP diabetic admitting last

History of Present Illness: 1 day prior to admission patient noticed to have increasing frequency of cough, associated with Difficulty of Breathing. Patient continue his medications, no consult done.Few hours prior to admission still with Difficulty of Breathing was immediately brought to our Emergency Room.

Past Medical History: (+)Hypertension (+)CHF (+)AAA

Family History: (-) Hypertension (-) Diabete mellitus (-)Cancer (-) Bronchial Asthma `