Ain Shams University Textbook of Surgery for Medical Students PDF

Preface This is the third edition of Ain Shams University Textbook of Surgery for Medical Students. The name of the book is changed from “Notes” to “Textbook”, as we believe the new name is a real description of the book, it is a textbook for medical students. This edition is totally revised and re...

Preface This is the third edition of Ain Shams University Textbook of Surgery for Medical Students. The name of the book is changed from “Notes” to “Textbook”, as we believe the new name is a real description of the book, it is a textbook for medical students. This edition is totally revised and re-edited so much so that some parts of the book are totally rewritten. We aimed at explaining every subject of the book in simple words to help medical students understand what they are reading and not simply to archive medical knowledge in their minds. The illustrations that we added to the text also help to achieve the goal from reading the book, that is understanding medicine rather than archiving medical knowledge. The names of the chapters are generally kept the same as previous editions, however, some new chapters are added such as the chapter of bariatric and metabolic surgery. The principles of operations are described in corresponding chapters but operative details are beyond the scope of this book. Editors Ahmed Abdel Aziz Abou Zeid Head of General Surgery Department Adel Abdel Aziz Ewada Professor of General Surgery  Acknowledgement The editors are greatly indebted to all staff members of the Department of Surgery, Ain Shams University, who contributed to writing this book. Without their efforts and dedication, this book would never have come to light. Many thanks are also due to contributing staff members from the Departments of Urology, Orthopedic Surgery, Plastic Surgery, Neurosurgery, Vascular Surgery, Pediatric Surgery, Cardiothoracic Surgery, Anaesthesia and Oncology, whose contributions aided in completing the chapters of this book, making it a complete and comprehensive textbook of surgery for medical students. The editors never forget the late Professor of Surgery, Abo Bakr El Sedik Mostafa, who was the first to adopt the idea of inviting all staff members of the Department of Surgery, Ain Shams University, to share in writing a textbook for medical students. The great effort that he made to fulfill this goal was completed by Professor Emam Fakhr, Professor Alae Abdalla and Professor Nabil Saber, Professors of Surgery, Ain Shams University, and two editions of the book were published over the last few years when they chaired the Department of Surgery. We thank them all.  Table of Contents Chapter 1 (Metabolic response to Surgery) ………..……………………………………………….……………. 1 Chapter 2 (Haemorrhage, Shock, Blood transfusion) …………………………………………………………. 5 Chapter 3 (Fluid, Electrolytes & Acid-Base Balance) ……………………………………………….…………. 25 Chapter 4 (Surgical Nutrition) …..………………………………………………………………………………………. 45 Chapter 5 (Surgical Infections) ….………………………………………………………………………………………. 53 Chapter 6 (Hand Infections) ……..………………………………………………………………………………………. 68 Chapter 7 (Preoperative Assessment & Preparation) ……..…………………………………………..……. 82 Chapter 8 (Wound & Wound Healing) …………………………………………………………………..…………. 90 Chapter 9 (Postoperative Care & Complication) …………………………………………………………..…. 100 Chapter 10 (Cysts, Tumours, Sinuses & Fistulae) ………………………………………………….…………. 109 Chapter 11 (Abdominal wall & Hernias) …………….……………………………………………………………. 125 Chapter 12 (Anaesthesia & Perioperative Care) …………………………………………………..…………. 143 Chapter 13 (Surgical Oncology) ………………………………………………………………………………………. 153  Part I (Basic Surgery); Chapter 1 (Metabolic response to Surgery) METABOLIC RESPONSE TO INJURY AND MULTIPLE ORGAN DYSFUNCTION Surgery, trauma and infection disturb the normal body physiology. Minor injury or infection leads to localized inflammatory response that is beneficial to the body, while major injury or infection leads to an exaggerated systemic inflammatory response that might be harmful to the body called systemic inflammatory response syndrome or (SIRS). SIRS affects every body system and organ and can eventually lead to multiple organ dysfunction syndrome or (MODS). MODS is a major cause of death in surgical patients and it is the most common reason for surgical patients to stay longer than 5 days in intensive care. Understanding these responses is essential to plan the appropriate intervention. Systemic inflammatory response syndrome (SIRS) Major adverse event such as major trauma, major operations, and major infection can cause major cell damage. SIRS is defined as an inflammatory state affecting the whole body in response to severe infectious or non-infectious insult. SIRS is initiated by the circulation of the noxious products of cell damage in the circulation. These include: - Inflammatory cells (macrophages and neutrophils) - Cytokines (IL8, TNF-α, IL1 and IL6) - Pro-inflammatory substances (prostaglandins, kinins, complement, proteases and free radicals) - Anti-inflammatory substances (anti-oxidants, protease-enzyme inhibitors and IL10) - Complement - Bacteria, bacterial products and toxins Such products are injurious to the capillary endothelium and their free circulation in blood can cause generalized endothelial damage. The capillary pores all over the body widen and the microcirculation will become “leaky”. Big protein molecules, that are normally confined to the intravascular space, will leak to the interstitial space dragging fluid with them causing hypotension, generalized hypoperfusion and oedema (see shock). MODS will eventually happen. Early on, the condition may be reversible, however later, irreversible organ failure will lead to death. Causes of SIRS - Major trauma - Major operations - Haemorrhage - Fluid loss and dehydration 1  Part I (Basic Surgery); Chapter 1 (Metabolic response to Surgery) - Infection, inflammation, major sepsis, endotoximia - Major cardiovascular events - Hypoxia - Ischaemia and ischaemia–reperfusion injury (see shock) In SIRS, two or more of the following criteria is met: 1- Temperature ≥38°C (100.4°F) or ≤36°C (96.8°F) 2- Heart rate ≥90 beats per minute 3- Respiratory rate ≥20 breaths per minute or 4- PaCO2 ≤32 mmHg or the need for mechanical ventilation 5- White blood cell count ≥12,000/μL or ≤4000/μL or ≥10% band forms Extra factors that contribute to the occurrence or worsening of SIRS Fall in Intra-vascular volume Hypothermia Pain Psychological Stress Starvation Multiple organ dysfunction syndrome (MODS) SIRS will eventually lead to MODS that is defined as progressive dysfunction of two or more major organ systems in a critically ill patient making it impossible to maintain homeostasis without external support. The sequence of individual organ failure in MODS often follows a predictable pattern with pulmonary failure occurring first, followed by hepatic, intestinal, renal and finally cardiac failure. Manifestations of organ failure in MODS are: - Pulmonary failure: Acute (formerly ‘adult’) respiratory distress syndrome (ARDS). - Hepatic failure: Rising bilirubin, serum glutamic oxaloacetic transaminase (SGOT) and lactate dehydrogenase (LDH) - Intestinal failure: - Bacterial translocation - Stress ulcer causing gastrointestinal haemorrhage requiring blood transfusion. - Renal failure: Rising serum creatinine and low urine output - Cardiac failure: Low cardiac output and hypotension. - Cerebral failure: Altered mental states - Disseminated intravascular coagulopathy (DIC). The mortality of MODS is related to the number of failing organs: mortality is 60% with two organs and more than 90% with three failing organs. 2  Part I (Basic Surgery); Chapter 1 (Metabolic response to Surgery) Components of the Metabolic Response to Injury The components of the metabolic response to injury include - Acute inflammatory response and cell damage - Effect on blood vessels and microcirculation - Effect on afferent nerves and sympathetic activation - Endocrine response to injury All these factors will be discussed in details in shock. SIRS and MODS in surgery Many surgical diseases or complications can lead to SIRS and MODS. Examples are severe acute pancreatitis, bowel anastomotic leak, major trauma, limb ischaemia, necrotizing fasciitis and others. Organ dysfunction often begins insidiously. If active resuscitation and treatment are not started promptly, by 7–10 days MODS will be established and the prognosis becomes substantially worse. Prevention and treatment of SIRS and MODS Prevention of SIRS and MODS is achieved by reducing the level of circulating injurious inflammatory mediators and limiting the period of stress. This can be achieved by eliminating the factors predisposing to the syndrome and improving the delivery of host body defences to the tissues. Prevention is achieved by: - Appropriate use of prophylactic and therapeutic antibiotics - Proper clinical judgement and early diagnosis before MODS is established - Proper surgical technique (effective excision of necrotic tissue, minimizing bacterial contamination, avoiding accumulation of postoperative fluid collections (serum or blood) - Surgical complications with septic potential should be treated early (e.g. drainage of abscesses, exteriorizing leaking anastomoses). It is often better to perform a laparotomy on suspicion and find it normal than to ‘wait and see’ and risk rapid deterioration and death. - Adequate and early fluid resuscitation in patients with hypovolaemia - Maintaining tissue oxygenation by supplemental oxygen or assisted ventilation as required. - Rapid resuscitation and early definitive treatment of major injuries - Early and thorough excision of necrotic and infected tissue - Rapid cardiovascular resuscitation and prevention of shock - Nutritional support, by supplemental oral feeding, fine-bore nasogastric tube, feeding jejunostomy, gastrostomy or by parenteral feeding (see chapter of Nutrition). Enteral feeding is preferred to nourish enterocytes and colonocytes. This helps prevention of 3  Part I (Basic Surgery); Chapter 1 (Metabolic response to Surgery) intestinal bacterial translocation. Glutamine, arginine and omega-3 fatty acids are believed to be important. - Proper pain control - Correction of any psychological stress - Warming patients and avoiding excess heat loss There is no specific treatment for established multiple organ failure. Management is by supporting organ systems with ventilation, cardiovascular support and haemofiltration/dialysis until there is recovery of organ function. 4  Part I (Basic Surgery); Chapter 2 (Haemorrhage, Shock, Blood transfusion) HAEMORRHAGE Definition: Haemorrhage is the escape of blood outside the circulatory system through the damaged wall of blood vessels. Aetiology: 1- Injury to a blood vessel due to mechanical or surgical trauma. 2- Involvement of blood vessels in surrounding pathology such as an overlying benign ulcer (e.g. duodenal ulcer eroding the gastroduodenal artery) or cancer (e.g. colon cancer eroding colonic wall vessels) 3- Congenital or acquired haemostatic defects (Haemorrhagic Diathesis) This can increase the amount of traumatic and pathological bleeding, or it can cause bleeding after minor or unnoticed trauma (spontaneous haemorrhage). Types Of haemorrhage: A – According to the type of bleeding vessel: 1-Arterial haemorrhage; is characterized by bright red jets of blood that rise and fall with pulse. 2-Venous haemorrhage; is characterized by dark red steadily flowing blood. Venous bleeding can be severe when large veins are opened or with high venous pressure. 3- Capillary haemorrhage; is characterized by bright red ooze of blood from a wide surface area. B- According to the timing of haemorrhage in relation to trauma: 1- Primary haemorrhage: Occurs at the time of injury or during operation. 2- Reactionary haemorrhage: Occurs within the first 24 hours after trauma or operation. It is caused by slipping of improperly tied ligature or dislodgment of a clot from a blood vessel. The latter is predisposed to by factors to such as normalization of arterial blood pressure after surgery, and postoperative increase in venous pressure due to cough or vomiting. 3- Secondary haemorrhage: Occurs 7-14 days after trauma or surgery and it is caused by sloughing of the wall of a vessel precipitated by factors such as infection (e.g. after haemorrhoidectomy), pressure necrosis from drains and malignancy. It can be fatal if a large artery is involved (e.g., 5  Part I (Basic Surgery); Chapter 2 (Haemorrhage, Shock, Blood transfusion) bleeding from the carotid artery after sloughing of the skin flaps of a radical neck dissection). C- Revealed (External) versus concealed (Internal) haemorrhage: Revealed or external haemorrhage is visible. It can occur through skin wounds or from body orifices (e.g. epistaxis and haematemesis) Concealed or internal haemorrhage is invisible. It can occur in body cavities (e.g., haemoperitoneum and haemothorax), or in interstitial tissue (e.g. haemorrhage around fractures). D- Acute versus chronic haemorrhage Acute haemorrhage means loss of blood in a short period of time. If considerable, it can lead to hypovolaemic shock. Common causes of acute haemorrhage are accidental and surgical trauma, gastrointestinal bleeding, and obstetric bleeding. Chronic haemorrhage means loss of blood over a long period of time. If improperly treated, it causes anaemia. Common causes include bleeding from chronic peptic ulcer and gastrointestinal malignancies. E- Surgical and non-surgical haemorrhage Surgical haemorrhage can be controlled by intervention, whether surgical operation or non-surgical intervention (e.g. angioembolisation and endoscopic control of haematemesis). Non-surgical haemorrhage is the general ooze from a raw surface due to coagulopathy. It cannot be stopped by any intervention. It requires correction of the coagulation abnormalities. Physiologic response to haemorrhage The physiologic response to haemorrhage has two aims: 1. To stop bleeding and 2. To maintain effective circulatory volume, the latter is directed to the perfusion of important organs and tissues (heart and brain) at the expense of less important organs and tissues (skin, skeletal muscle and splanchnic area). A. Physiologic response to stop bleeding: Vasoconstriction and retraction of the intima of the injured vessel. Formation of the platelet plug. Activation of blood coagulation mechanism. These mechanisms occur in sequence. They are more effective when the vessel is completely transected than when there is a side tear, and in traumatic than in pathological cases when 6  Part I (Basic Surgery); Chapter 2 (Haemorrhage, Shock, Blood transfusion) constriction of the vessel may be hindered by inflammatory or degenerative changes in the vessel wall or in its surroundings, e.g., the fibrous tissue in the base of a bleeding chronic peptic ulcer. B. Physiologic response to maintain effective circulatory volume: This is achieved by neural factors, endocrine factors and improved transcapillary refill: 1. Neural factors: Hypotension decreases stimulation of arterial baroreceptors (in the aortic arch and carotid sinus) and atrial stretch receptors leading to reduction of the normal inhibitory discharges in the vagus and glossopharyngeal nerves to the vasomotor center. The sympathetic system is thus stimulated resulting in: - Constriction of veins, which normally contain two-thirds of the blood volume. This displaces blood from the capacitance side of the circulation into the heart. - Constriction of arterioles raises the peripheral resistance. This involves mainly the arterioles of the skin, skeletal muscle, and splanchnic area. Perfusion of the heart and brain is maintained because their metabolic needs override the alpha-adrenergic vasoconstrictor discharge. - Increased rate and strength of cardiac contraction. 2. Endocrine factors: - Hypotension stimulates catecholamine discharge from the adrenal medulla and from the nerve endings throughout the autonomic nervous system. They increase the heart rate and myocardial contraction and cause constriction of the arterioles of the skin, kidney and viscera. - The metabolic hormones ACTH, cortisol, growth hormone and glucagon are increased. Insulin release is inhibited by adrenaline and noradrenaline. - Activation of the renin-angiotensin aldosterone system. The juxtaglomerular cells of the afferent renal arterioles secrete renin in response to renal hypoperfusion. Renin splits angiotensinogen to angiotensin I which is converted to angiotensin II by a converting enzyme in the lung. Angiotensin II is a powerful vasoconstrictor and stimulates sodium and water retention by a direct action on the kidney as well as indirectly through release of aldosterone from the zona glomerulosa of the adrenal cortex. N.B. Angiotensin-mediated vasoconstriction takes some 20 minutes to occur, whereas baroreceptor- vasoconstriction occurs within seconds. - Release of the antidiuretic hormone (vasopressin). Blood loss greater than 10% stimulates ADH release. ADH increases the permeability of the renal collecting tubules allowing water absorption into the hypertonic renal medullary interstitium. With severe haemorrhage high levels of ADH also cause vasoconstriction. 3. Transcapillary refill. Reduction of blood volume and constriction of arterioles causes a fall in capillary hydrostatic pressure and promotes movement of fluid from the interstitium into the 7  Part I (Basic Surgery); Chapter 2 (Haemorrhage, Shock, Blood transfusion) capillaries. The resulting haemodilution increases the blood volume and lowers its viscosity, thus improving effective circulatory volume. Clinical picture of haemorrhage Manifestations of haemorrhage depend on the amount of blood lost, the rate of loss and the patient’s cardiovascular reserve. Thus, loss of only 500 ml of blood may cause myocardial infarction in a patient with coronary artery disease, whereas in a healthy young adult, losses greater than 1500 ml may not even lower the systolic blood pressure. The following are the clinical manifestations of haemorrhage (and hypovolaemia): Symptoms: 1. Weakness and fainting especially when standing. 2. The patient feels cold and thirsty. 3. Haemorrhage may be evident (e.g. haematemesis, melena, bleeding external wound) Signs: 1. The patient is pale (due to constriction of skin blood vessels) and looks tired. The extremities are cold (again due to constriction of skin blood vessels) and clammy, the veins are collapsed and the capillary refill is slow. With decreasing cerebral perfusion, the mental status may vary from anxiety to drowsiness, but the patient usually remains alert. 2. Pulse and blood pressure. With mild blood loss (less than 500 ml), the pulse and blood pressure may remain normal, thanks to the efficient compensatory mechanisms. With more blood loss, tachycardia develops but the blood pressure remains stable. With further blood loss, however, the compensatory mechanisms can no longer maintain the blood pressure and progressive hypotension develops. 3. The pulse pressure decreases leading to a thready pulse. 4. There is tachypnea and air hunger. 5. There is hypothermia. Hypothermia predisposes to coagulopathy and it should be avoided. It can be aggravated by resuscitation by cold intravenous fluids. 6. Oliguria results from diminished renal perfusion. Classification of haemorrhage and estimating blood loss: The adult’s blood volume is 5 liters (70 ml/Kg in adults and 80 ml/Kg in children). Four classes of haemorrhage are recognized Class 1 < 15% of blood volume is lost Class 2 15–30% of blood volume is lost 8  Part I (Basic Surgery); Chapter 2 (Haemorrhage, Shock, Blood transfusion) Class 3 30–40% of blood volume is lost Class 4 > 40% of blood volume is lost In any patient with haemorrhage, it is of vital importance to have a rough estimate of the amount of blood loss. This can be determined from: 1. Clinical data. The more the amount of blood loss, the more severe is the clinical picture. 2. Type of injury. Haematoma around a closed fracture of the tibia contains 500-1500 ml of blood, that around a fractured shaft of femur, 500-2000 ml, that in fractured pelvis, 2000-3000 ml. Haemorrhage in abdominal or thoracic cavities can accommodate even more amount of blood. 3. Blood loss at operation is calculated by addition of the amount of blood in the suction reservoir and the amount mopped up by the swabs. Management of Haemorrhage Haemorrhage must be recognized and managed aggressively to reduce the severity and duration of shock and avoid death and/or multiple organ failure. The first priority is to arrest bleeding. Although necessary as supportive measures to maintain organ perfusion, attempting to resuscitate patients who have ongoing haemorrhage by fluid or blood transfusion will increase the blood pressure that will merely increase bleeding from the site, and fluid therapy cools the patient and dilutes available coagulation factors. Thus, operative haemorrhage control should not be delayed and resuscitation should proceed in parallel with surgery. A. Immediate resuscitative maneuvers 1. Stop external haemorrhage: Different measures can be done to stop external haemorrhage - Direct pressure can be applied on the bleeding site. Pressure can be maintained manually by a sphygmomanometer cuff or by a bandage. Tourniquet is contraindicated because of its complications unless the limb is going to be amputated. - Balloon tamponade can stop haemorrhage from oesophageal varices. - A bleeding cavity can be packed e.g. packing the nose in epistaxis. - Elevation of the limb above the heart level stops venous and decreases arterial bleeding. 2. Airway and breathing should be assessed and controlled as necessary. 3. A large bore cannula is inserted in a large peripheral vein, preferably in the upper limb, or by a cut down on the long saphenous vein, if necessary. This is used for taking blood samples and for intravenous infusion. The blood sample is tested for - Blood group, cross-matching and preparation of blood. - Coagulation profile is measured and corrected. 9  Part I (Basic Surgery); Chapter 2 (Haemorrhage, Shock, Blood transfusion) - Complete blood picture and haematocrit are measured for initial assessment and follow up. The initial haematocrit is often normal because RBCs and plasma are lost in the same ratio. Some 4-6 hours later, the haematocrit level will show a reduction because of haemodilution that is caused by movement of part of interstitial fluid into the circulation and replacement of the lost blood by crystalloids. 4. Insert Foley’s catheter to monitor urine output 5. Identify the site of concealed haemorrhage. The aim of this step is to define the next step in haemorrhage control (operation, angioembolisation, endoscopic control). At this point, according to the degree of haemorrhage, a decision should be made whether to take the patient immediately to intervention or to do investigations. The definitive management depends upon the cause of bleeding. B. Investigations Investigations must be appropriate to the patient’s physiological condition. Shocked patients and those with exsanguinating haemorrhage might not be suitable for any investigations more than rapid bedside tests. Patients who are not actively bleeding can have a more methodical, definitive workup by CT, ultrasound ……etc. C. Restore blood volume Patients should be aggressively resuscitated and warmed to avoid coagulopathy. Full correction should be the goal only after haemorrhage is controlled, before this correction aims at keeping the vital data acceptable to avoid patient’s deterioration and to bridge the time gap until active intervention to stop bleeding is taken. Volume replacement depends on the class of the haemorrhage. Class I haemorrhage does not need fluid replacement, class II needs to be corrected by crystalloids, class III and IV need blood transfusion. The amount of fluid infusion is 3 times the estimated deficit to replenish the interstitial fluid volume. Administration starts as bolus infusion for rapid correction of blood pressure then fluids are given at slower rate. Failure to achieve adequate improvement indicates inadequate replacement, continuing haemorrhage or associated pathology. D. General care and monitoring - Bed rest and analgesia - Monitor pulse, blood pressure, temperature, urine output, CVP, ECG, haematocrit, blood gases and blood lactate (index of anaerobic metabolism) - A pulmonary artery catheter is required in complex situations to monitor the function of the left side of the heart. 10  Part I (Basic Surgery); Chapter 2 (Haemorrhage, Shock, Blood transfusion) Shock Shock is the most common cause of death among surgical patients. Definition of shock Shock is defined as a systemic state of low tissue perfusion, which is incompatible with normal cellular respiration. If perfusion is not restored in a timely fashion, cell death ensues. Pathophysiology of shock A. Effect of shock on cells As perfusion to the tissues is reduced, cells are deprived of oxygen and must switch from aerobic to anaerobic metabolism. In anaerobic metabolism, glucose is utilized to produce a little amount of energy and lactic acid. The accumulation of lactic acid in the blood produces systemic metabolic acidosis. The little amount of energy is not enough for normal cellular function that eventually deteriorate. The Na/K pump of the cell membrane and intracellular organelles becomes inefficient, sodium and water accumulate in the cell and the lysosomes release autodigestive enzymes that cause cell lysis. Intracellular contents, including potassium, are thus released into the bloodstream. B. Effect of shock on blood and microcirculation As tissue hypoperfusion progresses, capillary circulation slows down causing activation of the blood coagulation cascade and the immune system. Thus, Unnecessary coagulation of blood occurs all over the body, this is called disseminated intravascular coagulopathy (DIC) and the natural body coagulation factors will eventually become depleted, this is called consumption coagulopathy. There will consequently be generalized bleeding tendency. Hypoxia and acidosis activate complement and prime neutrophils, resulting in the generation of oxygen free radicals and the release of cytokines. These molecules can injure the capillary endothelial cells that become ‘leaky’. The result is leakage of large protein molecules from the intravascular space to the interstitial space dragging with them huge amounts of fluid. This aggravates the hypovolemia, and the resultant tissue oedema exacerbates cellular hypoxia. C. Body defence mechanisms against shock - The cardiovascular system As preload and afterload decrease, the baroreceptors in the carotid sinus and aortic arch become less stimulated resulting in increased sympathetic activity and release of catecholamines from the sympathetic nerve endings and the adrenal medulla into the circulation. This results in tachycardia, increased cardiac muscle contractility and systemic vasoconstriction, all are factors helping to maintain the blood pressure. Vasoconstriction affects mainly blood vessels of the skin, muscle and splanchnic area, while blood supply to vital organs (brain and heart) is preserved. 11  Part I (Basic Surgery); Chapter 2 (Haemorrhage, Shock, Blood transfusion) - The respiratory system The metabolic acidosis and increased sympathetic activity result in an increased respiratory rate and minute ventilation to increase oxygen delivery to the tissues. Tachypnea also increases the excretion of carbon dioxide, causing compensatory respiratory alkalosis. - The renal system Decreased perfusion pressure in the kidney leads to reduced filtration at the glomerulus and a decreased urine output. The renin–angiotensin–aldosterone axis is stimulated resulting in further vasoconstriction, increased sodium and water reabsorption and conservation of bicarbonate trying to compensate for the metabolic acidosis. - The endocrine system The adrenal cortex secretes cortisol that causes sodium and water reabsorption in the kidney and sensitises the cells to catecholamines. The renin–angiotensin systems is activated and vasopressin (antidiuretic hormone) is released from the hypothalamus in response to decreased preload and results in vasoconstriction and reabsorption of water in the renal collecting system. D. Effect of shock on other systems Shock affects all body systems. Ischaemia of the gastric and duodenal mucosa may produce superficial ulcers, the so-called "stress ulcers" which may bleed. Translocation of bacteria and endotoxins can occur from the lumen of the colon into the circulation through ischemic mucosa. This can cause septic death in previously shocked patients even after resuscitation. ischaemic hepatic dysfunction and elevated liver enzymes is a frequent component of shock. E. Changes in arterial blood gases (ABGs) in shock: - Low pH (lactic acidosis) - Low P02