Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
45 Cards in this Set
- Front
- Back
|
Peritoneal cavity holes (6)
|
1. Esophageal hiatus: esophagus, vagus, esophageal vessels
2. Caval hiatus: CVC 3. Aortic hiatus: aorta, thoracic duct, azygos/hemiazygos vv. 4. Dorsal paired slits: sympathetic trunk/splanchnic n. 5. Inguinal canal: vaginal process/spermatic cord in male, round ligament in female; ext pudendal a/v, genital n. 6. R/L vascular lacunae: femoral a/v, lymphatics, saphenous n. |
|
|
Peritoneal cavity
|
parietal covers walls, visceral covers organs; largest extravascular space, 150% total skin surface area
|
|
|
Peritoneal membrane
|
single layer of squamous mesothelial cells, bidirectional semipermeable, contains processes and fenestrations, produce surfactant; supported by a cellular CT stroma
|
|
|
Peritoneal folds
|
mesentaries, omenta, ligaments- serous folds to bring vessels/nerves or support
|
|
|
Peritoneal fluid
|
dialysate of plasma (COP=28, TP 3g/dl, tncc=300, mostly macs)
|
|
|
Omenta:
|
milky spots” contain WBC’s
1. Greater= bursal (stomach-bladder), splenic (gastrosplenic l.), veil (L limb pancreas) 2. Lesser= lesser curvature stomach-liver (hepatoduodenal and hepatogastric l.) |
|
|
Retroperitoneal
|
kidneys, ureters, Ao, CVC, lumbar LN
|
|
|
Drainage
|
diaphragmatic lymphatics (R>L) w/ muscle contractions /neg intrathoracic pressure in cranial direction; particles <10um cleared rapidly mediastinal LN, thoracic duct, systemic circulation
|
|
|
Intra-abd pressure
|
(bladder)= 4.5 (2.0-7.5) cm H2O; incr from fluid, air can cause decr perfusion and incr thoracic pressure; generally incr after Xlap, decompression if >30cm H2O (if oliguric)
|
|
|
Peritoneum healing
|
mesothelium has rapid regeneration (cover in 4hr, new in 3d); adhesions occur with vascular compromise and inflammation
|
|
|
Defenses
|
1. Innate= peritoneal fluid (complement C3a and C5a) stimulate neuts chemotaxis, degranulation of basophils and mast cells
2. Specific= lymphocytes amply response to peritonitis (esp sepsis) |
|
|
Response
|
Activation of complement, humoral opsonins, antibodies
2. Lymphatic absorption 3. Neut and mac phagocytosis 4. Cytokines (TNF-α, IL-1β) initiate cascade, mesothelial cells produce IL-8, lymphocytes produce IL-6 and TNF-α = all proinflammatory = can measure severity of response Imbalance of factors, IL-10 attenuates and protects against lethal shock 5. Histamine and PG (mast cells/macs) cause vasodilation and incr vascular permeability exudation of fluid rich in complement, imunoglobs, clot factors, fibrin Peritoneal fibrinolysis system inactivated in inflammation (fibrin = adhesion formation) |
|
|
Adjuvants of peritonitis
|
Gastic mucin= heparin-like anti-complement effect
Bile salts= lower surface tension, alter cell adhesion, lyse RBCs release Hb Hb= interfers with phagocytosis, chemotaxis, killing, and clearance; provides iron for bacteria Fluid volume= incr bacterial prolif, slow clearance, incr mortality |
|
|
Systemic manifestations
|
Hypovolemia= protein-rich fluid into peritoneal cavity- hypotension and decr organ perfusion (MA and tissue hypoxia) – ARF, MDF
Hypoproteinemia= severe catabolism, incr BMR Sepsis: hyperdynamic state (incr insulin, glucagon, catecholamines), incr O2 consumption; endotoxins augment inflammatory cascade Fever: acute-phase reponse, enhances host defenses |
|
|
Localization
|
Omentum= isolates and seals source of contamination by adhesion
Ileus= sympathoadrenergic reflex inhibition (block myenteric cholinergic neurons), but incr bacterial translocation Reflex rigidity= diaphragmatic mm (decr respiratory movement, intraperitoneal circulation, and lymph clearance) |
|
|
Aseptic Peritonitis
|
Mechanical / FB= surgical exposure, gossypiboma, create granuloma/abscess
Starch granulomatous= Sx glove powder – now silicone based talcum Chemical= bile/urine – mild unless infected; gastric fluid is acidic and pancreatic enzyme autodigestion cause more severe inflammation Sclerosis encapsulating= encased in thick collagneous CT, +/- etiologic agents Parasitic= toxo, nymphal pentastomiasis, heartworm, mesocestoides |
|
|
Septic Peritonitis
|
GI contents= 60% - sx wound dehiscence MC (may be most lethal), also drug-induced perforation; severity changes with GIT site (worse colon)
Pancreatic abscesses= concurrent pancreatitis in 50% of peritonitis cases Urogenital= infected urine, pyometra, prostatic abscess – all rare Hepatobiliary= necrotizing cholecystitis, GB rupture, etc; survival 100% if clean bile, only 27% infected Peritoneal dialysis= 1/3 of dialysis cases, cloudy dialysate > 200cells/uL neuts |
|
|
Primary peritonitis
|
monobacterial, no inciting cause found, traditionally FIP (feline coronavirus)
|
|
|
Septic Peritonitis Physiology
|
Polymicrobial- E.coli / Bacteroides MC , (gram- endotoxins, esp alpha hemolysin- lowers pH, lyses RBCs, decr WBC recovery)
Often anaerobics (26% of time) |
|
|
Septic Peritonitis Dx
|
free gas on rads >70% with GI perf, (can persist 30d after surgery)
Tap: 20% + with 3ml/kg, 80% + with 10ml/kg, overall accuracy 43% 95% DPL DPL: 20ml/kg warm isotonic saline Cyto: WBC morphology (toxic/degen) and bacteria presence more important than wbc# Culture: blood culture bottles bedside: incr sensi from 42% - 91% Fluid chemistry: creat > serum (urine), bili > serum (bile); Glu <50 , lactate>2.5, low pH; Blood-fluid lactate <-2.0mmol/L = septic; Blood-fluid Glu > 20 = septic– (dogs only) cats lack glucokinase |
|
|
Peritonitis Tx
|
Ab= 3rd gen cephalosporin or ampi/AG – (28% gram+, 52% gram- sensi to fluoroquin)
Sx: lavage 200-300 ml/kg until fluid is clear, if not then leave open, repeat q24h Open vs closed- no diff survival, open group had more blood products, enteral feeding tubes, longer hospitalization (3.5 vs 6d) – but may be worst cases? Serosal patching / omentalization – but only experimental / anecdotal evidence Enteral feeding tube (early important)- consider NE, G, but J-tubes have 18-42% complication rate Heparin – low dose 100-200 U/kg SQ q 8h- improve clot function, bacterial clearance, decr fibrin formation in exp peritonitis |
|
|
Septic Peritonitis Prognosis
|
survival 50-80% (only 27% in septic bile peritonitis)
|
|
|
Cause - Dx peritonitis
|
Penetrating injuries – damage abdominal viscera 70%, with 50% GI perf (gunshot and bite wounds) – often colonize Pasteurella (bites) and Clostridium (guns)
Urine- severe metabilic, mild peritonitis, much worse if infected Chylous –High triglyds / chylomicrons on cytology Pseudochylous- high cholesterol (normal cell breakdown) normal triglyds Bicavitary effusions: incr with infectious and pancreatitis – incr mortality 3.3x Intra-Abscess: any organ, often anaerobes (Bacteroides) protected from defense mech Pneumoperitoneum: organ rupture, bacteria infection, urogenital leak, previous Xlap may persist for up to 30d (volume related) Hemoperitoneum: often spleen, liver, kidney – find in <50% traumas with Xlap; tap dx 50-60% accurate (will not clot) compare to serum PCV, 80-100% accurate DPL AbN sinus (fistulous) tracks: inhaled FB, contrast sinography + 60-87% sensitive Mesothelioma= older dogs/cats, reactive mesothelial cells, req. bx for dx |
|
|
True vs false hernia
|
True hernia= wall defects with hernia rings, peritoneal lining, from normal hole
False hernia= organs outside normal hole, NO hernia sac (initially) – trauma/incisional |
|
|
Hernia Parts
|
ring (thicken with scar), sac (mesothelial lining), contents (organs, fat)
|
|
|
Hernia types (based palpation)
|
Reducible (back to norm), incarcerated (irreducible) or strangulated (imped vascular)
|
|
|
Hernia principles
|
reduction, tension-free closure, obliteration (redundant sac tissue), local tissue (use)
Mesh: use when tension, extend 1.5-3cm past defect, integrates in 4-6 weeks with CT |
|
|
Umbilical hernia
|
Umbilical- MC, congenital result of failure/delay fusion of lateral abd folds (rectus m/fascia), (acquired umbilical rare), assoc with cryptorchidism, fucosidiosis, autosomal recessive
Omphalocele= large midline congenital umbilical defects, delay in GI loop transit to abd cavity, covered in amnion, rupture- death Breeds: Airedale, basenji, Peke, pointer, Weimaraner at risk, no gender Tx: spont closure <6 mo, 1-2cm defects= fix now, tiny/large repair with sterilization |
|
|
Caudal Abd-
|
Caudal Abd-
Indirect- enter cavity of vaginal process (through normal hole ~true hernia) - MC Direct (less common)- pass adjacent to rings (go where it wants! ~ false hernia) |
|
|
Inguinal
|
Inguinal- defect inguinal ring, small dogs(males) or older intact females (Shar-Pei, toy breed)
Inguinal canal:ext pudental a/v, genital n. Internal- rectus abd (med), int. abd. oblq m (Cr), inguinal ligament (lat/Cd) External- longitudinal slit in ext abd oblq m. aponeurosis Heritable – goldens, cockers, dachshunds; females (canal larger/shorter) Factors: enlargement of entrance to vaginal process – MC; bitches in estrus/pregnant (estrogen); assoc with perineal hernias in male dogs; weakening (nutrition/metabolic) Signs: bulge left > right, loss abd muscle detail, vomiting (predictive of GI contents), bilateral Sx: approach over hernia (conventional) – reduce, enlarge CrMed if needed, close primarily Midline – avoid mammary tissue, evaluate both sides, can extend to abd if needed Leave small bit of Cd aspect open to allow for neurovascular Complications= 17% (seroma, failure, infection); 3% mortality = great prognosis |
|
|
Scrotal-
|
Scrotal- indirect, defect in vaginal ring, into vaginal process, along sperm cord
Signs: young male dogs, often very large, assoc with ectopic testis/crypt Tx: repair now (high strangulation risk), approach over inguinal ring, or ventral midline if strangulated viscera; castrate concurrently |
|
|
Femoral-
|
Femoral- canal is lateral to inguinal ligament, hernia CdMed to vascular lacunae (femoral a/v, saph n) , near muscular lacunae (iliopsoas m/femoral n)
Signs: appear similar to inguinal hernia, but along the med thigh Sx: approach parallel to inguinal lig., ligate sac high in femoral canal, watch vessels |
|
|
Traumatic-
|
Traumatic- prone to adhesions/incarceration d/t lack serosal lining;
Sites: cranial pubic tendon, inguinal, paracostal, most have concurrent pelvic fx Rads: loss of abdominal strip, absence of organ, comorbidity Tx: delay unless ER problem, debride ischemic tissue, +/- drain; use autogenous tissue (Cr. sartorious m. flap) d/t infection/seroma potential Mesh: single, cuffed, double layer if tedious |
|
|
Incisional-
|
Incisional- (3-5d from Sx), d/t technique, interposed fat, infection, metabolic; no diff. between continuous vs interrupted if proper, (if questionable=interrupted)
Acute – stabilize, then repair immediately (evisceration) Chronic – challenging d/t lack of ID layers; “loss of domain” – abdomen used to smaller contents, hard to repair w/o prosthetics Complications: usually early, activity restrict (hobbles, etc) |
|
|
Diaphgragm:
|
Diaphgragm: central “Y” tendon and axial/abaxial mm.
Lumbar mm (paired) form R/L crus (Rt larger) bifurcate tendon insert medial to psoas mm. at 3-4th lumbar vertebra Costal m.: 13-8th ribs to central tendon Sternal m.: continuous with costal, from xiphoid to tendon Thoracic surface attached midline dorsal to esophagus, then deflects L along costal mm, back to midline at sternum; plica vena cava reflection attaches on Rt Blood: phrenic a. (from phrenicoabd) Nerve: phrenic (C5,6,7 dog; C4,5,6 cat) |
|
|
Congenital pleuroperitoneal
|
Congenital pleuroperitoneal: rare, dorsolateral part, open L crura, can be fatal
|
|
|
PPDH
|
Congenital Peritoneopericardial (PPDH): common (5-10%)- d/t faulty transverse septum, occur with sternal defects, Cr abd wall / umbilical hernia; may be asymptomatic
Signal: Weimeraner, DLH, Himalayan predisposed; PE: muffled auscult, enlarged cardiac silhouette with gas, no pleural effusion, Dx on echo Sx: midline celiotomy, adhesions rare, can use pericardium to patch if large defect Outcome: 14% mortality rate |
|
|
Traumatic
|
Traumatic: (85-90%)- sudden incr intra-abd pressure w/ open glottis
Normal P-P pressure gradient 7-20cm H2O, but incr >100 cm H20 on max inspire Rupture muscles (often costal) > tendon; Le ≥ Rt (15-20% bilateral); tears circumferential (40%), radial (40%) or combo (20%) in dogs, mostly circumferential (60%) cats Organs: liver (88%) > SI > stomach > spleen > omentum, etc Rt tears: liver, SI, pancreas / Le tears: stomach, spleen, SI Dx: 38% respiratory difficulty, muffled heart, shifted apex beat (80%), Rads- partial loss of D-line (97%), viscera in throrax (SI 61%, spleen/liver/stomach 35%), lung lobe collapse/effusion (20-31%), U/S helpful or GI contrast rads; 30% ascites with liver trapped Tx: Sx w/i 24hrs had 33% mortality (shock/MODS) Midline celiotomy +/- sternotomy, or lateral thoracotomy (pick side), or transsternal Serosal adhesions mature >7-14d; freshen hernia edges NOT needed, use 3-0 to 1 PDS/Vicryl continuous, watch CVC; can place cirumcostal sutures or advance diaphragm Patches: omenum, transversus abd/peritoneum (base 13th rib), > SIS, mesh Postop: no overinflation, reperfusion pulm edema if chronic; AB if liver/biliary injury Prognosis: survival 79% dogs, 76% cats, with delay (1-3wks) 90% survival, also with proper triage 80-94% survival; recurrence 4-5% |
|
|
Hiatal
|
Hiatal- Shar-peis, brachyocephalics with upper resp dz; usually intermittent (sliding); primary or secondary to gastroesophageal reflux major consequence (normally controlled by LES), may have abnormal esophageal motility, megaesophagus, acid reflux; may be para-esophageal
Dx: signs after weaning in congenital; fluoro with barium contrast Tx: Fix underlying cause!, tx medically with elevated feedings, H2 blockers, prokinetics 1st; fails 30d Sx Sx: 180° dorsal incision in phrenoesophageal lig (spare ventral vagus), retract Cd 2-3cm esophagus, ID LES Close diaphragm ventral to hiatus to 1-2cm diam esophagopexy (esophagus tunica muscularis to daphragm interrupted PDS Fundic gastropexy (slatter says via tube). NO Nissen fundoplication- it has huge complications (necrosis, fails, etc) |
|
|
Perineal Hernias
|
Signal: older, Bostons, boxers, pekes collie, corgi, OES, dachshund; males (female may have bigger levator m); 40% bilateral – 66% Rt, 34% left but both sides weak
Cats: 75% male, most bilateral, no sacrotuberous ligament Site: ext anal sphincter – levator ani MC, also levator – coccygeal m. (deterioration of levator ani m. common (neural, myopathy, hormonal), often intact males w/ prostatomegaly (11-43%); bladder retroflexion 20-25%- have incr enzymes; rectum (sacculates, dilates, flexure, deviates to side) Grade: 1= simple deviation, 2= + mild dilation, 3= severe dilation + bulge, impaction; also grade as simple unilat, bilat, or complicated (recurrence, grade 3 dilation, concurrent sx disease (prostate) or retroflexed bladder Tx: med – bulk laxatives (osmotic retain water), docusates (DSS – retain lytes, mucosal permeability); anti-androgen hormones (not recommended) Sx: Int obturator m. flap elevated lat-to-med, suture to ST lig or coccygeal m., watch sciatic when severing tendon of insertion, use 2-0 to 0 monofilament Colo/cystopexy alone inadequate; staged approach: lap 1st, >48h, herniorrhaphy 2nd Superficial glut transposition reflected 90 degrees to Cd Others: mesh, semitend, gracilis, subcutaneous perineal fascia recon, anal splitting Complications: wound infection 6-26% (E.coli) , incontinence 3-15%, fistula, prolapse 7-42%, sciatic neuropathy, bladder entrapment 30% mortality Recurrence: 8-18% w/i 1 yr, but 25% after (continued m. weakening); 2.7x incr if NO castration, also incr if re-op or inexperienced |
|
|
Uncomplicated – starvation
|
Early: hepatic glycogen glucose (8-12hrs) or 2-3d (Bojrab)
skeletal m. AA (deaminated) gluconeogenesis Neuroendocrine: decr BMR Lipolysis subst for glucose Liver ketogenesis (FA—incomplete oxidation acetate β-hydroxybutyrate & acetoacetate) Late: Fat fuel ketone bodies, muscle lactate (not AA) to liver gluconeogenesis |
|
|
Complicated – sick
|
1. Hypometabolic (ebb) shock phase - short
2. Hypermetabolic (flow) phase- catabolism of energy stores and lean body mass 3. Convalescent: Anabolic – tissue synthesis and repair Hormones: catecholamine, cortisol, ACTH glucagon,GH incr; insulin decr. – stimulated by neural input (esp trauma) --Incr BMR and proteolysis (neurohorm driven): glycogen rapidly depleted -- AA primary substrate (glutamine esp) Urine N2 loss reflect body mass catabolism, req. high protein intake to replace Fat primary energy substrate (glyercol / FFA) Glucose intolerance / hyperglycemia due to insulin resistance in tissues/liver |
|
|
Enteral nutrition:
|
ingesta maintains biliary secretion of IGA, decr bact translocat, prevent mucosal atrophy, maintain myoelectric activity, improves healing
Enterocytes derive 50% nutrients from lumen |
|
|
Parenteral nutrition:
|
Liquid: crystalline AA, emulsified lipids, dextrose, vitamins/ minerals; very Hyperosmolar
Central dedicated line (>600mOsm/L soln) Protein: 15-30% dog, 30-45% cat Carbs: <50% cats, >50% dogs Fats: 10-30% cats, 10-20% dogs Glutamine (nonessential AA)- depleted in sick, important for GI health, should supp. K: 20-30mEq/L, Phos 10-20mmol/L Complications- thrombophlebitis, hyperosmolarity, hyperglycemia, hyperlipidemia, sepsis |
|
|
Refeeding syndrome
|
hypophosphatemia results in RBC lysis; insulin drives K/P/Glu intracell – cardiac dysrhythmias
|
