Acute Abdominal Pain & Peritonitis - PDF

ACUTE ABDOMINAL PAIN. ACUTE ABDOMEN. ______________________ Dr. Kiril Draganov, MD, PhD, DSc, Prof. of Surgery Clinic of Liver, Biliary, Pancreatic and General Surgery ACC University Hospital „Tokuda“  Acute abdominal pain = AAP AAP may be the result of different causes, resp. diseas...

ACUTE ABDOMINAL PAIN. ACUTE ABDOMEN. ______________________ Dr. Kiril Draganov, MD, PhD, DSc, Prof. of Surgery Clinic of Liver, Biliary, Pancreatic and General Surgery ACC University Hospital „Tokuda“  Acute abdominal pain = AAP AAP may be the result of different causes, resp. diseases of: 1. abdominal organs - intra-, meso- or retroperitoneal; 2. retroperitoneal organs – for instance kydneys; 3. other organs and systems, for example:  CNS - meningitis, encephalitis, tumours, traumas;  thoracic organs – acute myocardial infarction, pleuritis, pneumonia, thoracis trauma  rheumatologic, hematogenous, endocrine, infectious diseases, toxic и др. Type of Causes Examples Characteristics Genesis pain Visceral 1. Increased 1. Biliary colic, urolithic  Not localized, around Irritation of intraluminal pressure; colic, intestinal obstruction the midline or the afferent (obturation); umbilicus; С-nerves: 2. Increased 2. Acute hepatitis, acute  Irradiation - possible; - in the intracapsular pancreatitis /oedema/, capsule of pressure; others.  No signs of parenchymato peritoneal us organs; 3. Catarrhal appendicitis, involvement; 3. Inflammation /initial cholecystits, diverticulitis; - in the wall of stage/;  blunt, hollow 4. Abdominal angina permanent/colici like; muscular 4. Ischemia; (mesenteric ischemia), organs “appendicular crisis”  Gradually increasing (inflammation), or 5. Different types of acute, sudden (biliary 5. Infiltration of carcinomas colic, ischemia); sensitive nerves Type of Causes Examples Characteristics Genesis pain Parietal Contact between  Destructive appendicitis  Exact location; Irritation of С- = visceral and/or and cholecystitis; and А-delta Somati c parietal peritoneum  Irradiation - possible; afferent and exudate, bile,  Perforation of a hollow nerves pancreatic secretion, muscular organ;  Peritoneal gastro-intestinal involvement – rebound on visceral + contents, urine, blood.  Rupture of graviditas tenderness ; parietal extrauterine, of a peritoneum parenchymatous organ  Gradual onset, crescendo type, or sudden, immediate;  Type of Causes Examples Characteristics Genesis pain Migratin Visceral pain   Acute catarrhal Characteristics of Irritation of А- parietal pain appendicitis or visceral pain get delta is added g to previous cholecystitis characteristics of irritation of C-  phlegmonous parietal nerves appendicitis or cholecystitis Spreadin The pathological  Perforated gastric or New regions are Irritation of С- process is spreading duodenal ulcer involved; regions with and А-delta on g visceral and in peritoneal spaces symptoms of parietal peritoneal involvement peritoneum in are spreading new regions Referred Different types of  Free gas/exudate/tumor Remote from the Merging intraperitoneal in the right subphrenic primary site (focus); afferent nerves pathological region  Right phrenic There is no from different regions processes nerve  pain in the right pathological process in shoulder, scapula the region of pain supraclavicular Type of pain Causes Examples Characteristics Genesis Visceral 1. Increased intraluminal 1. Biliary colic, urolithic colic,  Not localized, around the Irritation of afferent С-nerves: pressure; intestinal obstruction (obturation); midline or the umbilicus; -in the capsule of 2. Increased intracapsular 2. Acute hepatitis, acute  Irradiation - possible; parenchymatous pressure; pancreatitis /oedema/, others.  No signs of peritoneal organs; 3. Inflammation /initial 3. Catarrhal appendicitis, involvement; -in the wall of hollow muscular organs stage/; cholecystits, diverticulitis;  blunt, permanent/colici like; 4. Abdominal angina (mesenteric  Gradually increasing 4. Ischemia; ischemia), “appendicular crisis” (inflammation), or acute, 5. Different types of carcinomas sudden (biliary colic, 5. Infiltration of sensitive ischemia); nerves Parietal Contact between visceral  Destructive appendicitis and  Exact location; Irritation of С- and А- delta afferent nerves (Somatic) and/or parietal peritoneum cholecystitis;  Irradiation - possible; on visceral and parietal and exudate, bile,  Perforation of a hollow muscular  Peritoneal involvement – peritoneum pancreatic secretion, gastro- organ; rebound tenderness ; intestinal contents, urine,  Rupture of graviditas  Gradual onset, crescendo blood. extrauterine, of a parenchymatous type, or sudden, immediate; organ Migrating Visceral pain  parietal pain  Acute catarrhal appendicitis or Characteristics of visceral Irritation of А-delta afferent nerves is cholecystitis  phlegmonous pain get characteristics of added to previous appendicitis or cholecystitis parietal irritation of C-nerves Spreading The pathological process is  Perforated gastric or duodenal New abdominal regions are Irritation of С- and А- delta afferent nerves spreading in peritoneal ulcer involved; regions with on visceral and parietal spaces symptoms of peritoneal peritoneum in new involvement are spreading regions Referred Different types of  Free gas, exudate or tumor in the Remote from the primary site Merging afferent nerves from different regions intraperitoneal pathological right subphrenic region  Nervus (focus); There is no processes phrenicus dex.  pain in the right pathological process in the shoulder, right scapula region of pain  Acute abdomen = AcAbd AcAbd – syndrome with 5 characteristics and specific features: (1) Progressive worsening of patient’s general condition; (2) Abdominal pain; (3) nausea, vomiting (often, but not obligatory); (4) Flatus and stools discharge disturbances – it might be seized but diarrhoea may also be observed; (5) Symptoms of peritoneal involvement.  Acute abdomen Causes for AcAbd – 5 major groups: 1. acute inflammation - appendicits, cholecystitis, diverticulitis; 2. perforation of a hollow muscular organ – gastric/duodenal ulcer or cancer perforation, pressure ulcer (foreign body), HUHC, large intestine (during FCS); 3. Acute intestinal obstruction (Ileus); 4. Acute mesenteric vascular occlusion; 5. acute pancreatitis - a separate nosology because of its complex pathophysiology; it’s not included in.1.1. – acute inflammation N.B.! 1. AAP is not always a symptom of AcAbd, but there is no AcAbd without abdominal pain 2. AAP might be or might be not an indication for admitting the patient to a hospital, but AcAbd always necessitates hospitalization 3. AAP and AcAbd may arise:  suddenly, “de novo”, without whatever abdominal signs and symptoms;  in the development (evolution, clinical course) of an already existing disease. PERITONITIS ____________________________  Acute peritonitis – definition, characteristics Acute peritonitis = acute inflammation of visceral and parietal peritoneum with the following characteristics and specific features: 1. In most of the cases – secondary  another abdominal (more often) or extra-abdominal (rarely) disease; 2. Causes:  Chemical substances - gastric secretion, bile, pancreatic secretion, urine They cause initiation of aseptic inflammation - aseptic (chemical) peritonitis;  Bacteria – bacterial peritonitis; 3. Pathophysiology – severe local + generalized disturbances  MODS  Classification of acute peritonitis I. Focus present/absent – (1) primary = spontaneous – without a primary focus in the abdomen Examples: Alcoholic cirrhosis, Ascites (any cause), peritoneal dialysis, ventriculoperitoneal shunt (2) secondary = focal - a result of another pathological process (focus); (3) tertiary – acute peritonitis  apparent resolution even healing  recurrence within 48 hrs; II. Etiology – aseptic, bacterial, (fungal – usually complicating bacterial infection) III. Spreading in the peritoneal cavity: 1. Localized. 2. Diffuse – (2.1.) spreading and (2.2.) total) IV. Exudate: serous, sero-fibrinous, fibrinous, purulent, hemorrhagic, putrefactant; V. Phases of the disease – (1) initial, (2) toxic, (3) terminal (end-stage) V. Course of the disease – (1) acute; (2) chronic  Acute peritonitis Focus present or absent Secondary (more often) Primary (rare) Pathogenesis - intraperitoneal and less Pathogenesis - no primary focus often retroperitoneal process such as: exists intra- nor retroperitoneally. 1. Inflammation; 1. Hematogenous or lymphogenic 2. Perforation, rupture; route of infection – from a 3. Intestinal obstruction (bacterial distant but a known focus translocation); 2. Cryptogenic – no focus has 4. Trauma, incl. iatrogenic been identified Acute peritonitis – most common causes (primary focus  secondary peritonitis)  Secondary peritonitis (1)  Pathological process of an intra- or retroperitoneal organ: 1. Most common cause – inflammation of an:  intraabdominal organ – acute appendicitis, cholecystitis, diverticulitis;  retroperitoneal space and organs – purulent pyelonephritis + retroperitoneal paranephral phlegmone, acute pancreatitis.  Secondary peritonitis (2) 2. Disease  perforation or rupture:  Peptic ulcer - duodenal, gastric  Chronic ulcerative colitis  Rupture – urinary bladder, ovarian cyst, ectopic pregnancy  Perforated cancer – stomach, large intestine  Secondary peritonitis (3) 3. Intestinal obstruction (Ileus)  damaged mucosal barrier function  bacterial translocation No macroscopic perforation, but μ.o. pass into the peritoneal cavity per diapedesim (so called bacterial translocation) Ileus  ileus-peritonitis  Secondary peritonitis (4) 4. Trauma:  Penetrating abdominal trauma (stab or gun shot wounds) – infection is brought in the peritoneal cavity from outside.  Iatrogenic peritonitis – a type of secondary peritonitis with combined pathogenesis – traumatic (basic factor) + inflammatory (additional factor) Causes  different diagnostic and therapeutic procedures, such as ascites puncture, FNB, colon rupture in colonoscopy, urinary bladder rupture in cystoscopy, others.  Postoperative peritonitis  anastomotic leakage, intraoperative contamination, „foreign bodies” (for example gauze).  Primary (spontaneous) peritonitis No intra- nor retroperitoneal focus is found Pathogenetic mechanism № 1. (1) Primary focus exists but it is in a different anatomical region (site):  pleural cavity, mediastinum;  mouth;  bones, joints, (2) pathogenesis others. – hematogenous or lymphogenic spread Pathogenetic mechanism № 2. No intra- nor retro- nor extraperitoneal focus is found - “cryptogenic peritonitis”.  Acute peritonitis - pathophysiology Peritonitis = inflammation = local, defensive, multiple stage, stereotyped reaction of organism  inflammatory agent Inflammation (peritonitis) = biochemical, cellular and vascular reactions Basic pathological phenomena: - dehydration (hypovolemia); - inflammatory mediators (main role of cytokines); - toxicity; - circulatory insufficiency  tissue hypoperfusion and hypoxia; These phenomena - interdependent and aggravating; Finally (terminal stage)  MODS  MOF  Acute peritonitis - dehydration 4 main causes: (1) Fluid deposition in the splanchnic region:  exudate - extraintestinal;  intra-intestinal (third space) (2)  vomiting – “obligatory” symptom in every case of peritonitis; (3)  diarrhea – rare symptom, but may be seen in the initial stage of some diseases leading to peritonitis (4)   oral intake  Acute peritonitis – acute inflammation phases, mediators Acute inflammation (a local defensive stereotyped multiple stage Ireaction) phase: Tissue damage (necrosis) + mediator release  endogenous = tissue (Histamine, Serotonin) and = plasma mediators ( plasma kinins, complement, coagulation factors)  exogenous (released by the μ.o.) II phase: Vascular + cellular events  exudation  vasodilation   vessel wall permeability  blood cells (Neutr) and plasma elements migrate in the tissues III phase: Proliferation (Recovery processes) (extravasation)  vascular diameter and permeability are restored  exudate  lysis of necrosis  resorbed or excreted  Cytokines = immunomodulators Structure - oligopeptides (~5–20 kDa) Main function – give cell signals, i.е. regulation of inflammation Cytokines do not penetrate the cell membrane Action – bind to receptors  autocrine, paracrine and endocrine signals Many groups and the main of them are: сhemokines, interferons, interleukins, lymphokines and TNF  MF, B-Ly, T-Ly, Mast cells, Fibroblasts, endothelial and stromal cells  Acute peritonitis – circulatory collapse Sludge-phenomenon Cause  hypovolemia, hypotension and disturbed rheology (slowing down the blood velocity) + BAS (Histamine, Serotonin, Bradykinin) Pathophysiology: adhesion + aggregation + agglutination of blood cells  microcirculation is blocked  A-V shunts are the only and main route for blood Consequences:  Tissue hypoperfusion and hypoxia;  Anaerobic metabolism, acidosis;  Increasing toxicity;  MODS Acute peritonitis - Disturbed homeostasis, MODS, MOF Sludge phenomenon Tissue Adhesion, hypoperfusion aggregation, and hypoxia  aglutination anaerobic metabolism Dehydration and hypovolemia hypotension, disturbed acidosis, toxicity rheology Vascular wall paralysis  Acute peritonitis – classification based on According to the extent (scope involved) – acute peritonitis is classified as: spreading (1) Localized – the inflammatory process is circumscribed (enclosed) in 2 varieties:  Infiltrative mass (plastron) – periappendicular, perivesical, peridiverticular, etc.  abscess – circumscribed cavity filled with pus (2) Spreading = the inflammation has already started spreading: BUT inflammation affects ≤ 2 of 9 anatomical regions (3) Generalized = diffuse: Some authors distinguish 2 stages in the development of generalized peritonitis:  Diffuse peritonitis (spread in 3-5 anatomical regions);  Total peritonitis – all anatomical pouches, spaces, etc. contain exudate  Acute peritonitis – clinical presentation Clinical manifestation – depends on the causal factor (primary focus) In general - three stages: I. Initial (reactive) – up to 24th hour  Symptoms and signs resemble those of the causative disease  + gradual development of symptoms typical of peritonitis. II. Toxic stage – from 24th to 72nd hour.  the typical and marked symptomatology of peritonitis. III. Terminal stage – after the 72nd hour  in cases without treatment/ inadequate treatment  disturbed consciousness, development of MODS and later MOF  acute respiratory and cardia failure may  death.  Acute peritonitis – history 1. Severe, permanent abdominal pain:  sometimes – sudden abrupt onset, „like a stub wound“.  sometimes – gradually increasing, “crescendo” type.  In general – spreading from the primary site to new abdominal regions  in the toxic stage  diffuse pain;  lack of pain – alarming sign of terminal stage peritonitis or in exhausted anergic patients 2. Nausea and vomiting, without relief, painful hiccups 3. Stop of flatus and stools discharge  intestinal paresis (dynamic ileus). 4. Previous medical history  peptic ulcer? gall stones? Disturbances in flatus and stools discharge (colorectal cancer)  Acute peritonitis – general clinical signs (1) 1. Poor general condition, difficult/absent active movement, forced position; 2. CNS and consciousness:  Initial stage – euphoric, tense;  Toxic stage - lethargy and apathy  Terminal stage – coma; 3. Skin – pale, cyanotic, cold, clammy sweat,  turgor and elasticity; 4. Febrile (common sign), axillary/rectal To > 1оС (Lennander’s sign); 5. facies Hippocratica - hollow eyes, collapsed temple and brown, black, livid or lead colored face, dry lips and tongue  Acute peritonitis – general clinical signs (2) 6. Respiratory system - tachypnea, decreased vesicular breathing; 7. Cardiovascular system –  Initially - tachycardia without extensive hypotension (compensatory reaction)  Sometimes bradycardia  vagal nerve stimuli (perforated ulcer, biliary peritonitis);  Later – tachycardia, hypotension, weak pulse; 8. Liver and kidney failure: at the end of toxic and in the terminal stage:  jaundice;  Hemorrhagic diathesis – petechiae (purpura spots 1cm, suffusions (larger subcutaneous hematoma);   urine output;  Acute peritonitis – abdominal clinical signs Inspection  auscultation (unpainful method!)  palpation  percussion 1. Limited involvement and sparing of anterior abdominal wall in breathing 2. Hypoactive to absent bowel sounds („dead silence“) 3. Palpation and percussion – signs of peritoneal irritation (involvement):  abdominal wall rigidity  Plenies sign - pain at palpation and a painful tap in the right lower abdomen  Blumberg‘s sign = rebound tenderness - there is pain upon removal of pressure (or pain gets stronger) rather than application of pressure to the abdomen.  Signs of primary disease that has caused peritonitis, for example signs of acute appendicitis, acute cholecystitis, etc.  Acute peritonitis – diagnosis 1. History and physical examination; 2. Lab tests:  Severe inflammation -  WBC, Neutr,  CRP  Toxicity - disturbances of WEB and ABB, metabolic acidosis;  MODS – disturbed hemostasis;  bilirubin, ASAT, ALAT  urea,  creatinin 3. US, X-rays, CT scan 4. Laparocentesis - a form of body fluid sampling procedure (peritoneocentesis):  the peritoneal cavity is punctured by a needle to sample peritoneal fluid  polymorphonuclear (PMN) cell count > 250 cells per mm3  microbiological tests 5. Diagnostic laparoscopy  Acute peritonitis – differential diagnosis Three main aspects: (1) Diseases of abdominal organs that:  cause  peritoneal irritation and/or paralytic ileus;  do not cause peritonitis (2) Between different causes for peritonitis; (3) Extra-abdominal diseases that mimic “Acute abdomen” (Acute peritonitis)  CNS;  pleuro-pulmonaly diseases;  acute myocardial infarction  hematologic, rheumatologic, endocrine and other diseases.  Acute peritonitis – conservative treatment Aim: preoperative resuscitation (substitution, compensation, stimulation, Duration: etc.) as fast as possible, as effective as possible; simultaneous with diagnostics Treatment/prevention of: toxicity, disturbances in WEB and BAB, hemostasis, MODS. Activities: NGT, urinary catheter, CVL. Monitoring: (1) clinical, instrumental - consciousness, Т° С, breathing, PR, ABP, CVP, diuresis, NGT; (2) Laparotaroty – FBC, biochemical tests; (3) other instrumental – US for example Consists of: saline and carbohydrate solutions i.v., plasma expanders, blood and fresh frozen plasma infusion (if indicated); antibiotics, cardiotonics, diuretics,  Acute peritonitis – surgical treatment Primary importance, basic method of treatment Laparoscopy or Laparotomy Aims = main elements of the procedure: (1) Evacuation of exudate; (2) Primary focus surgery – for example appendectomy, cholecystectomy, perforated ulcer suture, hemicolectomy (perforated cancer or ulcer in chronic ulcerative colitis), sigmoid colon resection (diverticulitis); (3) Antiseptic solution installation – peritoneal cavity lavage with 3-5 L of antiseptic fluid (Jodine or Chloride solutions); (4) Drainage of peritoneal cavity  Acute peritonitis – principles of drainage Drainage of peritoneal cavity – a milestone in the treatment scheme! Principle – all spaces, gutters and pouches must be drained! А, В – left and right subphrenic spaces F, K – right and left paracolic gutters C, D – inter-intestinal space, ileo-cecal region, duodenojejunal recessus Е – Douglass pouch ACUTE APPENDICITIS ____________________  Acute appendicitis (AcAp) - statistical data, etiology AcAp = the most common cause for AcAbd (1) - 4-7cases/1,000 population/year Age – usually affects 10-40 year old patients Etiology Sexand pathogenesis –male/female = 1/2– 4 theories: (1) Enterogenic way of spreading infection; (2) Lymphogenic and hematogenic of spreading infection; (3) Neuro-vascular theory – vascular and smooth muscle spasm; (4) Immunogenic theory – Peyer’s patches (lymphatic follicles in the appendiceal wall) get hyperactive  inflammatory or neoplastic process in a neighboring structure/organ  Acute appendicitis – pathogenesis In general - pathogenesis of AcAp has the following pathway: (1) lymphoid hyperplasia – most often or fecalith, foreign body, tumor, worms - occasionally (2)  appendiceal stasis (= obstruction of the appendiceal lumen) (3)  bacterial overgrowth (4)  inflammation  Acute appendicitis – pathology (1) Pathology – 4 stages in the development of AcAp (1) catarrhal – edema, hyperemia, intralumenal pressure, intact muscularis and serosa (2) phlegmonous – ulcerated mucosa, microabscesses, ischemia, fibrin on the serosa (2’) appendiceal empyema = obturated lumen; filled with pus (3) gangrenous = necrotic wall  transmural infiltration + ischemia (4) gangrenous perforated  4.1., 4.2., 4.3. (4.1.) periappendicular inflammatory mass – the borders of the appendix can’t be clearly distinguished from other structures and organs (syn. = plastron appendicitis)  they attempt to circumscribe inflammation (usually front abdominal wall, Acute appendicitis – pathology (2)  Acute appendicitis – clinical manifestation (1) Typical symptoms of acute appendicitis: (1) initially - visceral pain (catarrhal appendicitis): dull pain centred around the navel, or epigastrium, moving to the RLQ - Kummel’s sign (from the navel) or Kocher’s sign (from the epigastrium) (2) later – parietal (somatic) pain: (phlegmonous appendicitis): shifts and progresses to a sharp pain in the lower right side of the abdomen. (3) much later – pain disappears (gangrenous appendicitis): due to necrosis (4) pain in the lower back (retrocoecal appendix) or in the pelvis (rectum) - less commonly (5) fever + rectal/axillary T > 0.5 °C = lower abdomen and/or pelvic inflammation (6) nausea, vomiting, loss of appetite.  Acute appendicitis – clinical manifestation (2) Typical signs of acute appendicitis: (1) General signs of toxicity/SIRS – flushed face, dry tongue, associated fetor oris. pyrexia (up to 38°C), tachycardia – common findings. (2) Abdominal examination:  no tenderness at palpation nor rebound tenderness – catarrhal appendicitis;  localised tenderness  muscular rigidity + guarding – phlegmonous stage;  pain has a punctum maximum in McBurney’s point (McBurney’s sign)  rebound tenderness (Blumberg’s sign);  Markle's sign (jar tenderness) - pain in the RLQ is elicited by the heel-drop test (dropping to the heels, from standing on the toes, with a jarring landing);  Acute appendicitis – clinical manifestation (3) (2) Abdominal examination (continued):  Rosenstein's sign, also known as Sitkovsky’s sign - tenderness in the RLQ increases when the patient moves from the supine position to a recumbent posture on the left side  Bartomier’s sign – pain on palpation when the patient is in left lateral position  iliopsoas sign or Cope’s sign – pain on extension of right hip (typical for retrocecal appendix)  obturator sign – pain on internal rotation of right hip  Larach’s sign - rigidity of right lumbar muscles (retrocecal or retroperitoneal appendix) Rovsing sign  Acute appendicitis – diagnosis, treatment  50% of cases = typical clinical signs  clinical manifestation +  30% of cases – oligosymptomatic  Lab tests +  20% – atypical, mimicking other diseases  US +/- CT scan  History – 3 symptoms  Physical exam - 3 signs  Lab tests – 2 criteria  Acute appendicitis – in childhood AcAp is a rare condition under 3 years of age :  The appendix has a broad ostium  no risk of appendiceal stasis  Underdeveloped intramural lymphatic structures AcAp is a dangerous disease in childhood : Quick development and  incompetent immune system; progress to destructive  relatively small peritoneal cavity forms  relatively small omentum Clinical presentation: (1) Toxicity and SIRS – prevailing symptoms and signs; (2) Vomiting, diarrhoea – leading symptoms  fast dehydration (3) Abdominal pain – often vague, not a leading symptom  Acute appendicitis – in elderly AcAp is a rare but dangerous condition in elderly patients :  comorbidity ( more underlying diseases) Atypical  sluggish bodily physiological reactions presentation  suppressed/inadequate immunity morbidity and Clinical presentation: mortality (1) “Silent” on set, general symptoms like acute viral infection; (2) Constipation – it’s seen in many elderly patients  misdiagnosed (3) Perforation  abscess or diffuse peritonitis are common complications (4) Postoperative morbidity - surgical wound infection, intraabdominal infections, others worsen the postoperative complications  Acute appendicitis – in pregnant AcAp is a rare but dangerous condition in pregnant women : Appendix’s site Atypical location changes during of pain, pregnancy Blumberg’s sign Clinical presentation: (1) “Silent” on set, symptoms resemble those of pregnancy course, just like abdominal pain, vomiting, general malaise; (2) Constipation – it’s seen in many pregnant women  misdiagnosed (3) US – the only appropriate diagnostic method