Gastrointestinal.docx

**[Gastrointestinal]** **[GI physiology]** **Saliva** Secreted by parotid, submandibular and sublingual glands in response to thought, smell, taste and presence of food - [Composition]: - 98% water - Remaining 2% include - Electrolytes -- lower Na+ but higher K+ concentration (hypotonic) - Resting pH is 7.0, but when HCO3- secretion is increased pH rises to 8.0 - Proteins and enzymes (mucin, haptocorrin, alpha-amylase, lingual lipase) - Bactericidal substances (thiocyanate, lysozyme, lactoferrin and IgA) - [Functions]: - Lubrification of food (mainly due to mucin) - Digestion - Alpha-amylase is an enzyme identical to pancreatic amylase, which catalysed the breakdown of carbohydrates polymers; it works optimally at pH 7 and manages to cleave up to 75% of starch before becoming denaturated by acidic environment in the stomach - Lingual lipase starts digestion of dietary triglyceride (++ important in neonates where pancreatic lipase is immature) - Haptocorrin is a protein that binds vitamin B12 protecting it from the low pH in the stomach - Neutralization of acid -- the HCO3- containing saliva dilutes and neutralizes gastric acid when the stomach content - Refluxes in the esophagus - Enters the oral cavity during vomiting (there is a large increase in salivation prior to vomiting) - Antibacterial effects - [Production]: salivary glands are composed of acinar cells and ducts surrounded by contractile myoepithelial cells. Production of saliva occurs in 2 phases - **Acinar cells**: produce the primary secretion by active transport of electrolytes, followed by passive movement of water - The primary secretion is approximately isotonic (Na+, Cl- and HCO3- similar to plasma) - **Duct cells**: modify the primary secretion to give a secondary secretion - Na+ and Cl- are reabsorbed - K+ and HCO3- are secreted - Reabsorption takes place at a greater rate than secretion and saliva becomes hypertonic - [Innervation of salivary glands] - Parasympathetic innervation -- stimulation produces vasodilation of blood vessels supplying the acini and myoepithelial cells contraction -\> secretion of mainly serous, electrolyte-rich saliva - Parotid gland is supplied by glossopharyngeal nerve (CN IX) with pre-ganglionic fibres synapsing at the otic ganglion - Submandibular and sublingual glands are supplied by facial nerve (CN VII) with pre-ganglionic fibres synapsing at the submandibular ganglion and post-ganglionic fibres travelling with the lingual nerve - Sympathetic innervation -- stimulation produces vasoconstriction of blood vessels and myoepithelial contraction -\> brief increase in secretion of mainly mucous saliva that is rich in amylase, followed by a period of decreased saliva production - [Salivary glands] - Sublingual gland -- produces mainly mucous saliva - Parotid gland -- produces mainly serous saliva - Submandibular gland -- produces mainly serous saliva **Swallowing** Complex process involving the coordination of a number of muscles, both voluntary and involuntary. Involves passing of a food bolus from the oral cavity to the oesophagus via the pharynx with closure of the larynx to prevent aspiration. Swallowing reflex is controlled by the swallowing centre in the medulla oblongata - [Phases]: - **Oral phase** -- only voluntary phase of swallowing - Food bolus is pushed against the hard palate by the tongue - Sensory information from the hard palate is fed back to the medulla via the glossopharyngeal nerve, which triggers the initiation of involuntary phases - **Pharyngeal phase** -- under involuntary control; the medulla coordinates - Closure of nasopharynx by soft palate - Protection of the laryngeal inlet (lateral cricoarytenoid, oblique and transverse arytenoid muscles) followed by abduction of the aryepiglottic folds (all these laryngeal muscles are supplied by the **recurrent laryngeal nerve**) - Elevation of the hyoid (by the digastric and stylohyoid muscles), which moves the larynx superiorly and anteriorly; in addition, the epiglottis moves downwards to direct the food bolus towards the posterior pharynx and away from the larynx - **Oesophageal phase** -- also involuntary - Once the food has entered the oesophagus, the upper oesophageal sphincter closes and the **lower oesophageal sphincter** (LOS) partially relaxes - The food bolus is propelled along the oesophagus by peristalsis. There are 2 types of [peristaltic waves] propagated by the enteric nervous system - ***Primary peristaltic waves***: initiated by the medullary swallowing centre during swallowing, and continues from beginning of the oesophagus to LOS, regardless of the location of food bolus - ***Secondary peristaltic waves***: initiated by the food bolus stretching the oesophagus wall - By the time peristaltic waves reach the LOS, it has fully relaxed to allow the food bolus to pass - Smooth muscles of the LOS then contract to prevent gastric contents refluxing into the oesophagus - The speed at which the food bolus moves along the oesophagus is much slowed (3 cm/s) than along the pharynx (30 cm/s) - [Functional anatomy of the oesophagus] - Muscular tube that transmits food from the pharynx to the stomach - Upper third has skeletal (striated) muscle, while the lower 2/3 has smooth muscle - Normal mucosa is stratified squamous epithelium - LOS is formed by tonic contraction of smooth muscle in the distal 2-4 cm of the oesophagus, as it passed through the diaphragmatic hiatus - While the upper oesophageal sphincter (cricopharyngeus) has a high resting pressure (up to 100 mmHg), the LOS has a much lower resting pressure - "**Barrier pressure**" = difference between LOS pressure (normally 20-30 mmHg) and intragastric pressure (normally 5-10 mmHg). It is reduced by - Swallowing - Pregnancy (LOS tone is reduced by progesterone and gravid uterus increasing intra-abdominal pressure) - Hiatus hernia (LOS is no longer aligned with the diaphragmatic opening and the acute angle between the oesophagus and the diaphragm is lost) - Drugs (many drugs reduce LOS tone -- alcohol, volatile anaesthetics, propofol, thiopentone, opioids, atropine, glycopyrrolate) - Metoclopramide, anticholinesterases (e.g. neostigmine) increase LOS tone - Non-depolarizing muscle relazants have no significant effect on LOS tone **Stomach** - [Functions]: - Temporary storage of large meals (slowly releasing food into the small intestine) - Secretion of digestive enzymes (e.g. gastrin) - Mixing (by vigorous contractions of gastric smooth muscles, which helps mixing and liquefying ingested food) - Secretion of gastric acid (to defend against ingested microorganisms) - Secretion of intrinsic factor (IF) (which aids the absorption of vit B12) - Endocrine (secreting hormones to control gastric emptying) - [Substances secreted by the stomach]: - **Hydrochloric acid** (HCl) -- secreted by the **parietal cells**, up to 150 mmol/L; secretion is promoted by 3 stimuli - **Histamine** which stimulates H2 receptors (most important stimulus for gastric acid secretion) - **Parasympathetic stimulation** through the vagus nerve (Ach acts as neurotransmitter at muscarinic M3 receptors) - **Gastrin** (least important stimulus but has an important indirect effect, triggering histamine release from neighbouring enterochromaffin-like \[ECL\] cells) - **Pepsinogen** -- pepsin is an important peptidase that starts the process of protein breakdown in the stomach. The proenzyme pepsinogen is secreted in the stomach lumen by **chief cells**, where it is converted to pepsin by the acidic environment. Chief cells are triggered to secrete pepsinogen by - Gastrin - Parasympathetic nervous activity (through the vagus nerve) - **Gastrin** -- peptide hormone secreted by **G cells** in the stomach in response to - Parasympathetic nervous activity (through the vagus nerve) - Distension of the stomach - Presence of partially digested proteins in the stomach - Stimulation of parietal cells to secrete HCl (both directly and through stimulation of histamine release from ECL cells) - Stimulation of chief cells to secrete pepsinogen - Stimulation of gastric motility - **IF** -- glycopeptide secreted by **parietal cells**, which has an important role in vit B12 absorption - Vit B12 is released from ingested animal proteins as they are broken down in the stomach - In the low-pH environment of the stomach, IF has a low binding affinity for vit B12, so very little is bound; release vit B12 is instead bound to **haptocorrin** (vit B12 binding protein) which protects the acid-sensitive structure of vit B12 - In the duodenum, vit B12 is re-released as haptocorrin is digested by trypsin, while IF is resistant to trypsin - In higher pH of the duodenum, IF avidly binds vit B12 - In the terminal ileus, IF receptors allow absorption of IF-vit B12 complex - **Mucus** -- **mucous cells** secrete a HCO3- rich mucus that covers the gastric mucosa with 2 main roles - Protection of gastric mucosa from the highly acidic contents of the stomach lumen - Lubrication of the stomach wall, protecting it from frictional damage due to vigorous peristalsis and mixing of partially digested food - [Secretion of gastric acid from parietal cells] - Parietal cells are triangular-shaped epithelial cells of the gastric mucosa. Key features are - Close proximity to ECL cells - Extensive network of secretory canaliculi - H+/K+-ATPase pump - 3 stimulatory receptors: histamine H2, Ach and gastrin - 1 inhibitor receptor: somatostatin - Carbonic anhydrase (CA) within the cell cytoplasm - Main stimulus for secretion of gastric acid is histamine, synthetized and stored by ECL cells that release histamine in response to gastrin or parasympathetic stimuli - Histamine acts by increasing cAMP concentration within the parietal cell - Gastrin and Ach also directly stimulate parietal cells, but to a lesser extent than histamine - Mechanism for gastric acid secretion is - CO2 diffuses into the parietal cell from the blood - CO2 reacts with water to give H2CO3 in a reaction catalysed by CA - H2CO3 dissociates in H+ and HCO3-, which go separate ways - **Apical membrane**: **H+/K+-ATPase** actively pumps H+ into the secretory canaliculi in exchange for K+ (proton pump) - **Basolateral membrane**: HCO3- is exchanged for Cl- (HCO3- enters the blood where it causes a measurable increase in blood pH whenever gastric acid secretion is stimulation -- alkaline tide) - Cl- diffuses down its concentration gradient through Cl- channel to the secretory canaliculi - K+ also diffuses down its electrochemical gradient back into the secretory canaliculi through a K+ channel - [Phases of gastric secretion]: there are 3 phases - **Cephalic phase**: around 30% of total gastric acid secreted per meal is produced in response to anticipation, smell and taste of food - Vagus nerve activity results in secretion of HCl, gastrin and pepsinogen - **Gastric phase**: gastric distension triggers gastrin release from G cells, which in turn stimulates pepsinogen release from chief cells, histamine release from ECL cells and HCl secretion by parietal cells - 60% of gastric acid is secreted during this phase - **Intestinal phase**: once the acidic chyme enters the duodenum, **secretin** is released from the duodenal mucosa, which reduces the acidity of the chyme by - Stimulating pancreatic **ductal cells** to secrete HCO3-, thus increasing the pH of the chyme - Inhibiting gastrin release from G cells, thus reducing the amount of acid produce by parietal cells - [Control of gastric emptying]: rate of gastric emptying into the duodenum depends on - *Consistency of chyme* -- liquid pass through the stomach much faster than solids; the pyloric sphincter constricts when solids come close, preventing them from leaving the stomach until they are liquified - *Volume of chyme* -- increased gastric volume promotes gastric emptying - *Content of chyme* -- protein enters the small intestine most rapidly, followed by carbohydrate, while fat is associated with the slowest gastric emptying - *Duodenal distension* -- results in a reflex inhibition of enteric nervous system, reducing gastric emptying - *Acid* -- low duodenal pH triggers release of secretin from the duodenal mucosa which promotes pancreatic HCO3- secretion and inhibits gastric secretion; as gastrin is responsible for stimulating gastric motility, reduced gastrin concentration slows gastric emptying - *Fat* -- **cholecystokinin** (CCK) is secreted by the duodenal mucosa in response to presence of duodenal lipid; CCK increases the tone of the pylorus, reducing gastric emptying, which allows the small intestine to have more time to digest the lipids - *Hyperosmolarity* -- hyperosmolar chyme passing into the duodenum inhibits gastric emptying through a complex enteric nervous system reflex - *Sympathetic nervous system activity* - *Pain* - *Drugs* (e.g. opioids) - *Diseases* (diabetic autonomic neuropathy, acute abdomen, ileus) - [Time needed for gastric emptying]: depends on whether the gastric contents are solid or liquid - **Solids** -- after consuming a typical meal, there is a 20-30min periods with minimal gastric emptying; this lag period allows for mixing of food with gastric secretions and for pepsin to start breaking down proteins. After 30 min, the rate of gastric emptying is approximately linear, resulting in a steady decrease in gastric volume - **Liquids** -- clear liquids empty from the stomach exponentially, without a lag phase. However, if the fluid is hyperosmolar, acidic or contains fats, the rate of gastric emptying will be slower and may mirror the non-exponential pattern of solid food ![](media/image2.png) **Vomiting** Involuntary, forceful, rapid expulsion of gastric content through the mouth. Usually preceded by nausea, an unpleasure upper abdominal sensation. - [Control of vomiting]: vomiting is coordinated by the **vomiting centre**, an anatomically ill-defined area in the medulla oblongata - Vomiting centre is in close contact with 3 important structures - Respiratory centre - Nucleus tractus solitarius (which receives afferent information from various cranial nerves) - Chemoreceptor trigger zone (CTZ) (located on the floor of the 4^th^ ventricle of the medulla, in the area postrema) - CTZ is located outside of the BBB and receives blood directly from the systemic circulation - Many inputs to the vomiting centre can trigger nausea and vomiting - **CTZ**, which has many stimulatory receptors - Dopamine (D2) - Serotonin (5-HT3) - Ach - Opioid - Substance P (NK-1) - **Cranial nerve VIII** -- which carries information from the vestibular system (involved in travel sickness) and involves - Muscarinic receptors - H1 receptors - **Cranial nerve IX** -- carries afferent information from the pharynx (input involved in the gag reflex) - **Enteric nervous system and cranial nerve X** -- carries afferent information from the GI system (GI mucosal cells stimulate vomiting centre through activation of serotonin 5-HT3 receptors in response to distension, infection, chemotherapy and radiotherapy) - **Higher centres** (e.g. limbic system) -- can also initiate vomiting in response to anxiety and extreme emotional states - In response to emetic stimuli, the vomiting centre coordinates the parasympathetic nervous system, sympathetic nervous system and motor neurons to produce a characteristic series of events that results in expulsion of gastric contents through the mouth - [Sequence of events involved in vomiting]: divided in 3 phases - **Pre-ejection phase** -- consisting of - Nausea - Decreased gastric motility - Reverse peristalsis of the small intestine (which pushes proximal small bowel contents back into the stomach) - Secretion of HCO3- rich saliva (mediated by parasympathetic nervous system) - Sweating and tachycardia (mediated by sympathetic nervous system) - **Retching phase** -- consisting of - Deep inspiration followed by closure of the glottis, which protects the trachea from aspiration of gastric contents - Rhythmic contractions of the intercostal muscles, diaphragm and abdominal muscles against a closed glottis; the alkaline contents of the proximal small intestine are vigorously mixed with stomach contents, thereby increasing pH of gastric fluid - The increased intrathoracic pressure compresses the oesophagus, preventing reflux of stomach contents - **Ejection phase** -- consisting of - Continuation of glottic closure - Contraction of pylorus, which pushes gastric contents into the body and fundus of the stomach - Relaxation of LOS and oesophagus - Sudden, dramatic increase in intra-abdominal pressure, resulting from contraction of abdominal muscles and descent of the diaphragm (this pushes gastric contents completely out of the stomach and into the oesophagus) - Soft palate occludes the nasopharynx, and reverse peristalsis rapidly expels oesophageal content out of the mouth **Absorption and digestion** - [Accessory organs involved in digestion]: - Teeth and tongue -- involved in initial mixing of food with saliva - Salivary glands, liver, gallbladder and pancreas -- secrete substances involved in chemical and enzymatic breakdown of food - [Anatomy of the small intestine]: divided in 3 parts (duodenum, jejunum and ileum) - Most dietary nutrients are absorbed in the jejunum with some exceptions - Vit B12 and bile salt in the terminal ileum - Iron in the duodenum - Dietary fat and water throughout the small intestine - Small intestine is made up of 4 layers - **Adventitia** -- outermost layer, composed of loose connective tissue - **Muscularis externa** -- outer layer of longitudinal smooth muscle and an inner layer of circular smooth muscle - **Myenteric plexus** (part of the enteric nervous system) lies between these muscle layers, where it coordinates smooth muscle contraction - **Submucosa** -- contains nerve cells making up the **Meissner's plexus** (secondary enteric nervous system plexus), blood vessels, lymphatic vessels and elastic connective tissue - - **Mucosa** -- innermost layer, divided into (from outermost to innermost) - *Muscularis mucosae*: layer of smooth muscle that provides continuous agitation of the mucosa, increasing contact with luminal contents and preventing their adherence - *Lamina propria*: which contains blood vessels and collections of immune cells - In the **ileum**, the immune cells are organized into lymphoid nodules, called **Peyer's patches** - *Epithelium*: absorptive cells of the intestine, called enterocytes - The absorptive surface of the small intestine is increased by - ***Valvulae conniventes*** -- mucosal folds that project into the lumen of the small intestine - ***Villi*** -- tiny finger-like projections of the intestinal wall - In between villi are **goblet cells** which secrete mucous, and **intestinal crypts** which secrete brush border enzymes and contain stem cells - ***Microvilli*** -- microscopic projections on top of the villi (**brush border**) - Each villus has 3 vessels: - Single arteriole (that gives rise to a capillary network at the tip of the villus) - Single venule (where the capillary network drains, returning blood to the liver through the portal vein) - Single lacteal (lymphatic capillary which transports absorbed dietary fats as chylomicrons to the thoracic duct) - [Digestion and absorption of carbohydrates] - Dietary carbohydrate polymers (e.g. starch) must be broken down into their constituents monosaccharides before they can be absorbed - **In the mouth** -- digestion of carbohydrates begins in the mouth where ***salivary amylase*** breaks down complex carbohydrates into small carbohydrates polymers and monosaccharides - **In the duodenum** -- ***pancreatic amylase*** continues the breakdown of complex carbohydrates - **At the brush border** -- specific ***brush border enzymes*** (sucrase, maltase, lactase), integral membrane proteins attached to the villi, hydrolyse the smaller carbohydrate polymers into their constituent monosaccharides - **At the enterocyte** -- once carbohydrate has been broken down, the resulting monosaccharides can be absorbed by the enterocytes - *Glucose and galactose*: can only be absorbed by secondary active transport through Na+ co-transporter (**sodium-glucose linked transporter, SGLT1**) which requires a low enterocyte intracellular Na+ concentration, generated as a result of basolateral Na+/K+-ATPase pump activity - *Fructose*: absorbed by facilitated diffusion - *Pentose sugars*: absorbed by simple diffusion - **Within the enterocyte** -- once absorbed into the enterocytes, glucose and galactose travel down their concentration gradients and pass through the basolateral membrane and into the capillary by facilitated diffusion (via the **transmembrane glucose transporter, GLUT-2**) - As monosaccharides are osmotically active, their absorption across the enterocytes also results in absorption of water - [Digestion and absorption of proteins] - Ingested proteins must be broken down into single amino acids, dipeptides and tripeptides before absorption - **In the stomach** -- protein digestion begins. Proenzyme pepsinogen is release by chief cells in the stomach and, at low pH, is converted to pepsin. Pepsin cleaves the peptide bonds of dietary proteins, resulting in shorter polypeptides - **In the duodenum** -- protein digestion continues. 2 important peptidases of pancreatic origin (**trypsin** and **chymotrypsin**) cleave polypeptides, resulting in dipeptides and tripeptides - **At the brush border** -- peptidases cleave dipeptides and tripeptides into single amino acids - **At the enterocyte** -- single amino acids are absorbed in a similar way to glucose, but there are different co-transporters for neutral, basic and acidic amino acids - Short peptides (2 or 3 amino acids) are also absorbed by secondary active transport using an H+-linked co-transporter system - **Within the enterocyte** -- short peptides are broken down into single amino acids which then exit the enterocyte by facilitated diffusion across the basolateral membrane - Amino acids are osmotically active and water molecules are also absorbed - [Digestion and absorption of lipids] - The main dietary lipid is triglyceride, with small amounts of phospholipids, cholesterol and fat-soluble vitamins - Triglyceride must first be broken down into its constituents (glycerol backbone with 3 fatty acid residues) before being absorbed - **Emulsification in the duodenum** -- lipids are insoluble in water and, therefore, triglyceride tends to aggregate in large droplets when exposed to aqueous environment in the GI tract - **Emulsification** = **bile acids** (secreted by the liver and store and released from the gall bladder) coat the lipid droplets, diving them into smaller droplets - **Enzymatic breakdown of triglyceride** -- **pancreatic lipase** acts to hydrolyse each triglyceride molecule into 2 free fatty acid molecules and 2 monoglyceride - However, pancreatic lipase can only act on the surface of lipid droplets (bile acids divide them into smaller droplets, increasing the surface are for pancreatic lipase to act) - **Micelle formation** -- the free fatty acids and monoglycerides combine with **bile salts**, forming micelles - **At the enterocyte** -- when a micelle makes contact with an enterocyte, the lipid contained within it is absorbed by simple diffusion - The bile salts remain in the gut and are absorbed in the terminal ileum, where they return to the liver and are recycled - **Within the enterocyte** -- monoglycerides and fatty acids travel the endoplasmic reticulum (ER) where they are recombined to form triglyceride. This is then packed with cholesterol, phospholipid and a cellular label called **apolipoprotein** to form **chylomicrons**. - Chylomicrons are released from the enterocytes into lacteals and flow through the lymphatic system until they are released into systemic circulation at the thoracic duct **Pancreas** Has both endocrine and exocrine functions, but most of the pancreatic tissue is dedicated to secretion of pancreatic fluid while the islets of Langerhans, which produce glucagon (alpha cells), insulin (beta cells), pancreatic polypeptide (PP cells) and somatostatin (delta cells), occupy only 1-2% of the pancreatic mass. - [Role of pancreatic secretions in digestion] - Pancreatic juice drains into the duodenum through the pancreatic duct - Main cell types of exocrine pancreas are - **Acinar cells** -- produce digestive enzymes - **Trypsinogen and chymotrypsinogen** - Upon entering the duodenum, proenzyme trypsinogen is cleaved by the duodenal enzyme **enterokinase** in trypsin, a powerful peptidase - Trypsin then cleaves both chymtotrypsinogen and more trypsin (**autocatalysis**), resulting in exponential increase in peptidase activity - Trypsin also activates other pancreatic proenzymes (phospholipase A2 and elastase -- important for the pathogenesis of pancreatitis) - **Pancreatic alpha-amylase**: which catalyses the hydrolysis of large polysaccharides to smaller carbohydrates polymers - **Pancreatic lipase**: catalyses hydrolysis of triglyceride to free fatty acid and 2-monoglyceride - **Ductal cells** -- secrete HCO3- and water - **HCO3**-: neutralises gastric acid entering the duodenum, allowing the right pH for pancreatic enzymes to work - HCO3- synthesis uses CA in a similar manner to gastric acid secretion but HCO3- diffuses down its concentration gradient into the lumen of the pancreatic duct in exchange for Cl- which return to the lumen of the pancreatic duct through a separate Cl- channel (CFTR), while H+ is expelled from the ductal cell across the basolateral membrane into the capillary by exchange with Na+. The exchange of H+ and Na+ is driven by the low intracellular Na+ concentration generated by the Na+/K+-ATPase pump - HCO3- is osmotically active and its movement is accompanied by water - [Control of pancreatic secretions] - Between meals there is very little secretion of pancreatic fluid but, when food enters the stomach and, particularly, when chyme enters the duodenum, secretion of pancreatic fluid is strongly stimulated - Secretion of pancreatic fluid has both neural and humoral control mechanisms - **Neural**: pancreas is innervated by the **vagus nerve** that, when activated during the cephalic phase of digestion, results in a small increase in pancreatic acinar cell activity - **Gastrin**: secreted by G cells of the stomach in response to gastric distension and, as well as stimulating gastric acid secretion by the parietal cells, also stimulates pancreatic acinar cells to secrete digestive enzymes in preparation for the arrival of carbohydrates, proteins and fats (***feed-forward control system***) - **CCK**: secreted by the duodenal mucosal cells in response to a fat- or protein-rich chyme entering the duodenum; as well as increasing production of bile by the liver and slowing gastric emptying, CCK also stimulated the pancreatic acinar cells to secrete digestive enzymes (***negative-feedback control system***) - **Secretin**: hormone secreted by the duodenal mucosa in response to presence of acid-containing chyme in the duodenum; as well as slowing gastric emptying, it also stimulates duct cells of the pancreas to secrete HCO3- to neutralise the chyme. **Intestinal motility** - [Difference of intestinal motility in the fed and fasted states] - **Fed state**: small intestinal contractions are designed to - Promote mixing of chyme with digestive enzymes and bile salts - Propel chyme along the small intestine to the large intestine - **Fasted state**: there are infrequent, irregular contractions of the small intestine - Every 90 min there is a period of intense coordinate intestinal contractions, spreading from the duodenum to the ileocecal valve (**migrating motor complex, MMC**) - It takes about 90 min for the contraction to sweep along the length of the small intestine, moving undigested chyme towards the colon - [Intestinal contractions during the fed state] - **Segmental contractions**: contraction of the circular smooth muscle in neighbouring segments which compartmentalises a section of the bowel and is followed by continuous contraction and relaxation of the longitudinal muscle, which results in the mixing of chyme with digestive enzymes rather than propulsion along the GI tract - Segmental contractions also bring chyme in contact with the brush border, promoting nutrient absorption - **Propulsive contractions**: highly coordinated contraction of the circular muscle behind the food bolus and longitudinal muscle, resulting in propulsion of chyme along the GI tract - Each peristaltic wave lasts only a few seconds, travelling at only a few cm per second - [Control of intestinal motility] - The smooth muscle cells of the small intestine have a negative RMP (-40 to -70 mV) - Contractions of the smooth muscle occur when the membrane potential exceeds threshold potential; opening of voltage-gated channels allows a sudden influx of Na+ and Ca2+, which depolarizes the cell membrane and stimulates contraction - Normally, the smooth muscle cell membrane potential fluctuates 20-30 times per minute, in a pattern called **slow waves** - These fluctuations in cell membrane potential are insufficient to exceed threshold potential by themselves but they help to coordinate depolarizations and contractions of the GI tract - Slow waves may originate from the **interstitial cells of Cajal** (ICC) in the myenteric plexus - Presence of food bolus stretches the intestinal walls and triggers release of neurotransmitters, which cause a small depolarization of the cell membrane - The threshold potential is exceeded when the next slow wave occurs, resulting in a **spike potential** -\> muscle contraction is triggered - Small intestinal motility is influenced by inputs from both the nervous and endocrine systems - **Enteric nervous system** -- consists of efferent and afferent neurones, converging on 2 types of ganglion - **Myenteric (Auerbach's) plexus** - **Submucosal (Meissener's) plexus** - *Sympathetic nervous system* -- through synapses in the prevertebral ganglia, causes **inhibition** of enteric nervous system -\> reduces intestinal motility and GI secretions, as well as reducing blood flow to the gut by splanchnic vasoconstriction - *Parasympathetic nervous system* -- through the vagus nerve, causes **stimulation** of intestinal motility and GI secretions - **Endocrine system** -- many hormones are involved in the control of gastric motility, but the control of intestinal motility is less understood - **Motilin** -- hormone released from the **duodenal mucosa** every 90 min during fasting and is responsible for stimulating the MMC - Stimulus for release of motilin is unknown - Erythromycin is a motilin agonist, with pro-kinetic effect - **Vasoactive intestinal peptide (VIP)** -- has multiple effects on the GI tract - Increases secretion of water and electrolytes in the small intestine - Stimulates intestinal motility Molecule Produced in... Target is... Motility effects? ---------------------------- ---------------------------------------------------- -------------------------------------------------- ---------------------------------------------------------------- Gastrin G cells of stomach (antrum), duodenum and pancreas Enterochromaffin like cells, parietal cells Stimulates gastric contractions Secretin S cells of SI (duodenum mainly) Pancreas and stomach Inhibits gastric emptying, stimulates gall bladder contraction CCK I cells of SI, some neurons in brain and GIT Gastric smooth muscle, gall bladder and pancreas Inhibits gastric emptying, stimulates gall bladder contraction Motilin M cells of SI Gastric and duodenal smooth muscle Stimulates MMCs Gastric inhibitory peptide K cells of SI Pancreatic beta cells None (some sources say mild decrease in gastric emptying time) Glucagon like peptide SI endocrine cells Pancreatic endocrine cells Slows gastric emptying **[Acute abdominal pain]** [Causes] of abdominal pain - Distension of hollow viscus or organ capsule - Ischemia - Traction - Inflammation N.B.: IVDD may also result in abdominal pain, although direct palpation of the area of spinal pain usually elicits more response **Diagnostic evaluation** Inpatients that develop abdominal pain should have prompt review of their medical records followed by: - CBC - Biochemistry - Urinalysis - Radiographs - Abdominal POCUS - Radiographic contrast study - Abdominocentesis (or peritoneal lavage) - Response to treatment - +/- Exploratory laparotomy ***Signalment and history*** - FB or infectious diseases in young animals - Prostate disease in older intact male dogs - Pancreatic exocrine insufficiency in young adult GSD can predispose to mesenteric volvulus - String FB common in cats - Acute pancreatitis common in middle-aged, obese female dogs Ask for history of exposure to toxins, dietary indiscretion, ingestion of FB, other affected animals in the household, previous medical history, previous medications, history of trauma, vaccination status ***Physical examination*** Detailed abdominal palpation may occasionally locate the specific area of pain (but many times this cannot be specified) ***Clinical pathology*** - Database: PCV, TS, BUN, smear, venous blood gas, electrolyte levels - High PCV and TS -\> dehydration - Normal or high PCV with low/normal TS -\> possible protein loss - AHDS is associated with high PCV (60% to 90%) and normal/low TS - Low PCV and TS -\> hemorrhage - But PCV may be normal initially due to splenic contraction (dogs) and before dilution - Most common causes of hemorrhage in dogs with abdominal pain: splenic rupture, GI ulceration - Most common causes of hemoabdomen in cats: non-neoplastic (54%) and neoplastic (46%) - Blood glucose - High if DM caused by acute pancreatitis - BG is rarely \>200 mg/dL in dogs with extreme hypovolemia secondary to abdominal or GI hemorrhage, presumably as a result of catecholamines on glycogenolysis and gluconeogenesis - Increased BG in cats may be associated with stress or diabetes - Low BG often associated with sepsis (more typically in the 40-60 mg/dL range) - Hypoadrenocorticism may also be a cause of low BG - BUN (dipstick in the US) - Increased due to prerenal, renal (pyelonephritis) or post-renal (ureteral/urethral obstruction) causes - Disproportionately high BUN compared to creatinine -\> possible GI hemorrhage - Blood smear - Assess at low power for PLT clumps first - PLT count under oil immersion: normally 8-15 PLT per oil immersion field (100x) - Each PLT in the monolayer is equivalent to approximately 15,000 PLT/uL - If there are \>2-3 PLT per field, it is unlikely the bleeding is strictly the result of thrombocytopenia - Decreased PLT is one of the most consistent findings in animals with DIC - RBC evaluation - Anisocytosis, macrocytosis and polychromasia -\> regeneration - Schistocytes (fragment RBCs) -\> suggest DIC - Heinz bodies -\> often seen in systemically ill cats and dogs with zinc ingestion (which may also cause pancreatitis!!) - WBC evaluation - Assess at lower power to get estimate of WBC number - Assess at higher power to evaluate morphology - Band cells indicate a more severe inflammatory or infectious process - Absence of leukocytosis or left shift does not rule out inflammatory/infectious process - Leukopenia can result from decreased production or sequestration, viral infection (e.g. parvovirus), immunosuppressive agents - Venous blood gas - Hypochloremic metabolic acidosis + hypokalemia and hyponatremia in animals with vomit due to upper GI FB - Hyperchloremic and/or lactic metabolic acidosis often present with diarrhea and hypoperfusion ***Abdominal imaging*** - Abdominal radiographs - Assess density, shape, size and location of all organs in the peritoneal and retroperitoneal space - Loss of abdominal detail - DDX: lack of fat in puppies or very thin animals, free abdominal fluid, pancreatitis, large mass(es) or carcinomatosis - Assess for free gas (without prior abdominocentesis or recent abdominal surgery) - perforation or presence of gas-forming organisms - Free gas is detected between the stomach or liver and the diaphragm in lateral radiographs - Horizontal beam radiograph with the animal in left lateral recumbency and focused on the last dependent area can increase the sensitivity for identifying free gas - A large volume of free gas is often associated with: pneumocystography of a ruptured urinary bladder, ruptured vagina, recent abdominal surgery, ruptured GDV, pneymoperitoneography, extension of pneumomediastinum (most commonly associated with pneumoretroperiteum) - A small volume of free gas is often associated with rupture of GI tract or infection with a gas-forming organism - Gas in gallbladder wall, liver or spleen is often associated with Clostridium spp infection - Segmental gaseous or fluid distension of the small bowel -\> suggests intestinal obstruction - Normal diameter of small intestine in dog is approx **2-3 times the width of a rib** (or less than the width of an intercostal space) - All the small bowel loops should have similar diameter - Abnormal for one segment to be 50% larger than another - Feline small intestine should not exceed **twice the height of the central portion of L4** vertebral body (or 12 mm) - Generalized small bowel distension -\> suggests generalized ileus or distal GI obstruction - Consider repeating radiographs 3 hours later - if the bowel remains distended in the same are suggests obstruction - However, a recent study indicated serial radiographs do not significantly increase the accuracy of diagnosis of GI mechanical obstruction due to occult FBs (?) - Upper GI positive contrast study with barium - Severe intraperitoneal inflammation and granuloma formation can occur if barium leakage occurs as a result of bowel rupture - Can be minimized if surgery and abdominal lavage is performed shortly after - Abdominal ultrasound - More sensitive and specific than abdominal radiographs - Gold standard for detecting free fluid - Abdominal CT - Performs well in detecting acute pancreatitis in dogs, abdominal masses, bowel obstruction ***Abdominal fluid analysis*** By abdominocentesis (blind or US-guided) or by diagnostic peritoneal lavage - Compare creatinine and K+ of fluid vs blood if uroabdomen suspected - Higher in abdominal effusion - Compared BG and lactate on fluid vs blood if septic peritonitis suspected - Blood-to-abdominal fluid BG gradient **\>20 mg/dL** - 100% sensitive and specific for septic peritonitis in dogs - 86% sensitive and 100% specific in cats - Blood-to-peripheral lactate gradient of **2 mmol/L** or more - 100% sensitive and specific for septic peritonitis in dogs - Compare bilirubin and bile acids on fluid vs blood if bile peritonitis suspected - Higher in abdominal effusion - Fluid types based on cell count and total protein concentration - Pure transudate - Grossly clear - TP \5000-7000 cells/uL (mainly neutrophils, septic or nonseptic) - Presence of intracellular bacteria confirm septic peritonitis ![TABLE 109.1 Summary of Some Objective Diagnostics Used in the Approach to the Acute Abdomen Test Blood glucose minus peritoneal glucose for diagnosis of septic peritonitis Peritoneal fluid lactate minus blood lactate for diag- nosis of septic peritonitis Dogs abdominal ultrasound: small intestinal lumen dilation Fluid to blood potassium ratio for diagnosis of uroabdomen Fluid to blood creatinine ratio for diagnosis of uroabdomen Fluid to blood bilirubin ratio for diagnosis of bile peritonitis (also may see bile pigment/crystals in abdominal fluid) Dogs: ratio of maximal small intestinal diameter to the narrowest width of L5 on lateral radiograph Cats: ratio of maximal small intestinal diameter to the height of cranial endplate of L2 Specific cPLl (serum) for diagnosis of pancreatitis Specific fPLl (serum) for diagnosis of pancreatitis SNAP CPLI (serum) for diagnosis of pancreatitis SNAP fPLl (serum) for diagnosis of pancreatitis Diagnostic Criteria mg/dl \>2.0 mmol/L Jejunal luminal diameter of \>1.5 cm with normal wall layering Dogs: ratio of 1.41 Cats: ratio 1.91 Dogs: ratio 21 Cats: ratio Ratio \>1.6 Ratio \>2.0 \400 mcg/L: pancreatitis likely \5.3 mcg/L: pancreatitis likely Spot intensity test Spot intensity test Sensitivity Dogs: 100% Cats: Dogs: 100% Cats: not reported Not reported but should aggres- sively investigate for intestinal obstruction Dogs: 100% Cats unknown Dogs: Cats unknown Dogs: 100% Cats unknown Not reported but suggestive of small intestinal obstruction Not reported but suggestive of small intestinal obstruction 82% with severe pancreatitis, 63.6% with less severe pan- creatitis 67% in all cats with pancreatitis and 100% in cats with moder- ate to severe pancreatitis Specificity Dogs: 100% Cats: 100% Dogs: 100% Cats: not reported Not reported but luminal diame- ter not dilated then intestinal obstruction not likely Not reported but considered di- agnostic for uroabdomen Dogs: 100% Cats: unknown Not reported Not reported but suggestive of small intestinal obstruction Not reported but suggestive of small intestinal obstruction 96.8% 100% ](media/image4.png) [Pascual et al, JAAHA 2022] - case report of a dog with gall bladder rupture and bile peritonitis with normal serum bilirubin, low abdominal fluid bilirubin and no pigments - But bile acids were significantly higher in abdominal effusion than serum [Pascual et al, ECVIM congress 2020 ] - Dogs with biliary peritonitis had significantly higher fluid to serum bile acid ratio vs dogs with other causes of abdominal effusion - Abdominal fluid bile acid concentration was 100% sensitive and specific for biliary tract rupture (cut off of 769 umol/L) - Fluid to serum bilirubin ratio was not significantly different between groups **Surgical vs nonsurgical medical management** - Indications for immediate surgery - Abdominal wall perforation - Septic peritonitis - Persistent abdominal hemorrhage - Intestinal obstruction - Intestinal FB causing pain or bowel obstruction - Uroperitoneum - Free abdominal gas (not associated with recent surgery, pneumomediastinum, or invasive procedures) - Abdominal abscess - Ischemic bowel - GDV - Mesenteric volvulus - Bile peritonitis **[Regurgitation and vomiting]** **Differentiation of vomiting and regurgitation** Vomiting: premonitory signs, active abdominal contractions, presence of bile Ptyalism is seen as a result of nausea in vomiting patients or due to pooling and/or inability to swallow saliva in animals with regurgitation Animals with esophageal disease may regurgitate saliva frequently yet remaining bright and systemically healthy TABLE 1 18.1 Comparison of the Key Features of Vomiting and Regurgitation Vomiting Regurgitation Premonitory signs (nausea) often No premonitory signs seen (hypersalivation, depression, discomfort) Active abdominal contractions May occur at any time Digested food Bile may be present Passive ejection of food Typically occurs shortly after ingestion of food Undigested food, may conform to the cylindric shape of the esophagus No bile **[Regurgitation]** ***Definition*** Passive ejection of food, water or saliva associated with esophageal or, less commonly, pharyngeal disease ***Clinical consequences*** - Aspiration pneumonia - Significant negative prognostic indicator in patients with megaesophagus - Measures to reduce its occurrence: feeding strategies, amended anesthetic protocols, elevation of the head in recumbent patients - Weight loss Most patients are otherwise able to maintain good hydration ***Differential diagnoses*** More common in dogs than in cats Most commonly results from diseases of the esophagus or pharynx, but can also results in some cases from systemic diseases (e.g. laryngeal paralysis-polyneuropathy complex in young dogs) - Idiopathic megaesophagus - Most common cause of regurgitation in middle age to older dogs - Focal myasthenia gravis - Predisposed breeds: GSD, Golden Retrievers, Abyssinian, Somali, Siamese - Hypothyroidism - Epidemiologic evidence supporting an association is lacking ![BOX 1 18.1 Important Differential Diagnoses for Regurgitation Pharyngeal Disease Cricopharyngeal achalasia Focal or generalized neuromuscu- lar disease Foreign body Neoplasia Esophageal Disease Hypomotility: Mega esophagus Congenital Idiopathic (primary) Secondary Organophosphate toxicity Inflammation: Esophagitis Drug: chemical-induced Gastroesophageal reflux General anesthesia Hiatal hernia Idiopathic Lupus myositis Spirocerca lupiinfection Mechanical Obstruction Australian Tiger Snake Enven- omation Myasthenia gravis (20% to 30% of cases) Generalized neurcrnuscular d ase Hypoadrenocorticism Lead toxicity Hypothyroidism Dysautonomia Lower esophageal sphincter achalasia Esophageal stricture Foreign body Recurrent gastric dilatation Neoplasia Vascular ring anomalies Extraluminal compression (e.g., mediastinal mass) Hiatal hernia Gastroesophageal intussusception ](media/image6.png) ***Diagnostic approach*** - [History]: - Access to drugs or caustic substances, recent drug therapy or anesthesia - Drug-induced esophagitis due to doxycycline (but possibly also other drugs) - Odynophagia (pain on swallowing), repeated exaggerated swallowing attempts, lip smacking, arching of the neck - Less most commonly in patients with esophagitis, less in patients with megaesophagus - In the absence of odynophagia, most patients maintain a good appetite and attempt to eat the regurgitated ingesta - Other systemic signs: lethargy, anorexia, vomiting and diarrhea are not seen in patients with uncomplicated esophageal disease - [Physical examination]: thorough oral examination and palpation of the neck - Neck abnormalities: masses, palpable esophageal dilation, pain - Differentiate crackles over lung fields from sounds of fluid in the esophagus - [Clinical pathology]: routine CBC and biochem are usually unremarkable or show changes due to the underlying cause for megaesophagus - [Diagnostic imaging]: - Thoracic radiographs - can be diagnostic in case of megaesophagus or esophageal FBs; may show evidence of aspiration pneumonia, mediastinal masses, or congenital abnormalities (e.g. vascular ring anomaly) - +/- contrast study - Endoscopy - Abdominal ultrasound - rarely provide useful information - [Further diagnostic testing]: - Acetylcholine receptor antibody assay (on serum) - ACTH stimulation test - Serology for antinuclear antibody - Serum creatinine phosphokinase activity - Muscle and nerve biopsy - Thyroid function (TSH, fT4 and tT4) - but evidence of association with hypothyroidism is lacking ***Treatment*** Most animals are stable and well hydrated and do not require emergency treatment - these patients may be treated on an outpatient basis - Histamine-2 receptor antagonist or PPIs - to reduce risk of secondary esophagitis - Sucralfate may be added in patients having an active esophageal ulceration - Metoclopramide and cisapride (smooth muscle prokinetics) have no beneficial effects in dogs as the esophagus is almost exclusively made of striated muscle - Moreover, these agents could decrease the transit of ingesta to the stomach by increasing lowed esophageal sphincter tone - In cats, the caudal third of the esophagus is made of smooth muscle - although prokinetics (e.g. cisapride) may in theory be more useful in this species, primary esophageal dysmotility is uncommon in cats - Sildenafil and local injection of botulism toxin A - increase lower esophageal sphincter relaxation - Treatment of secondary aspiration pneumonia - Oxygen therapy - Broad-spectrum antimicrobials (ideally after airway sampling) - Feeding strategies - High calories diet in small, frequent meals from an elevated or upright position - Diet consistency should be tailored to the animal (some patients may have faster esophageal transit when fed a more liquid diet) - Temporary or permanent gastrotomy tube (in animals that cannot maintain adequate nutritional intake via oral route) - Esophageal tubes have been used for intermittent suction of the esophageal content to reduce the risk of aspiration pneumonia (but not adequate for feeding) ***Prognosis*** Fair in animals with congenital idiopathic megaesophagus - With adequate caloric supplementation and prevention of aspiration pneumonia, many animals develop improved esophageal motility over several months Morbidity and mortality associated with acquired idiopathic megaesophagus remains high - Patients with an underlying disease that can be treated may have a better prognosis **[Vomiting]** ***Definition*** Forceful ejection of upper GI contents May result due to gastric, intestinal or systemic diseases ***Physiology*** The vomiting reflex is mediated by the **vomiting center** in the **medulla** - Vagal and sympathetic afferent pathways from the GI tract transmit impulses to the vomiting center when stimulated by inflammation or overdistension - The vomiting center also received stimulation from within the brain - Vestibular system, cerebrum, chemoreceptor trigger zone - **CRT** is a specialized region (area postrema) located on the flood of the 4th ventricle and lacks an intact blood-brain barrier (therefore, it is sensitive to several common drugs and toxins) - Sufficient stimulation of the vomiting center results in initiation of vomiting - A period of intestinal antiperistalsis is followed by a highly coordinated sequence of events, beginning with a deep inspiration and ending with a strong simultaneous contraction of the diaphragm and abdominal wall musculature, and relaxation of the lower esophageal sphincter Anticipation ENK Cerebral Cortex Afferent neuron 02 Apomorphine Uremic toxins Hepatotoxins Endotoxins Cardiac glycosides 5-HT3 M, NKI Chemoreceptor trigger zone 5-HTIA Vomiting center 5-HT4 GUT MOT ENKg,6 Motion HI M, NMDA Vestibular system 2 Efferent neuron ***Clinical consequences*** - Dehydration and/or hypovolemia, as a result of fluid loss in the vomit and reduced fluid intake - Electrolytes and acid-base imbalances - Hypochloremic metabolic alkalosis - due to loss of gastric content rich in hydrogen and chloride ions, with or without a contraction alkalosis (most common with GI FBs) - Metabolic acidosis - as a result of dehydration - Mixed acid-base disorders - Hypokalemia - Aspiration pneumonia (less common with vomiting than with regurgitation because reflex closure of the glottis normally occurs during emesis) - Higher risk in animals that are laterally recumbent or have impaired laryngeal function or decreased level of consciousness ***Differential diagnoses*** Primary GI tract disease vs non GI tract disease (usually also have other clinical signs) Acute vs chronic vomiting ![](media/image8.png) ***Diagnostic approach*** - [History]: determine approximate frequency and duration, presence of fresh or digested blood (\"coffee grounds), vaccination status, travel history, medication history, dietary indiscretion or recent diet changes, drug or toxin exposure, any possibility of FB ingestion - [Physical examination]: - Thorough abdominal palpation (for pain or discomfort, effusion, organ distension, masses, FBs) - Oral exam (for uremic or ketotic odors, ulcers or linear FB) - Palpate thyroid gland in cat for a goiter - Rectal examination (to look for hematochezia, helminths, prostatomegaly with or without pain) - Assessment of hemodynamic status and hydration - [Clinical pathology]: - Full CBC and biochemistry (if normal, more suggestive of primary GI disease) - Electrolytes and acid-base status - Urinalysis (to differentiate renal vs prerenal azotemia) - Fecal sample submitted for zinc flotation and bacterial culture - [Diagnostic imaging]: - Abdominal radiographs - to rule out GI obstruction - +/- barium contrast radiograph - Abdominal ultrasonography - greater accuracy for identifying small intestinal obstruction than radiographs; may also assist in the identification of neoplastic obstructions and allow for assessment of other abdominal organs, evaluation of intestinal wall thickness and layering - Thoracic radiographs - to rule out esophageal diseases, primary or metastatic neoplasia in the thorax, assessment of heart and pulmonary vasculature, signs of aspiration pneumonia ***Treatment*** - Treatment of underlying cause - Treatment of electrolyte and acid-base disturbances - Fluid therapy - Symptomatic control of further vomiting - Withhold food for first 24-48 hours - To avoid further vomiting and let the GI tract rest to prevent development of food aversion in nauseated patients and reduce risk of aspiration pneumonia - Food should always be withheld in patients with suspected GI obstruction - However, some vomiting patients may have a significantly quicker recovery when early enteral nutrition is started and starvation may be unnecessary for some dogs and cats **[Esophageal foreign bodies]** **Most common foreign bodies**: bones, followed by treats, balls, toys, fish hooks, wooden stick **Most common location**: caudal esophagus between heart base and diaphragm, followed by cranial esophagus, thoracic inlet, heart base **Clinical signs**: vomiting, gagging, chocking, retching, anorexia, foaming, coughing, gulping **Diagnostics**: radiographs, ideally in right lateral recumbency **Reported complications**: esophagitis, esophageal tear, aspiration pneumonia, esophageal stricture, pneumothorax, pneumomediastinum, pleural effusion, pyothorax, hemothorax, pneumonitis, bronchoesophageal fistula, CPA **Negative prognostic factors**: - Longer time from ingestion to FB removal -\> worse mucosal damage, with longer pressure causing necrosis and possible perforation **[Savary-Miller classification of esophagitis]**: - Grade I: single erosion - Grade II: confluent erosions - Grade III: circular, confluent erosions - Grade IV: esophageal ulceration, stenosis or perforation [[Barash et al, JVIM 2022]](https://onlinelibrary.wiley.com/doi/epdf/10.1111/jvim.16383) - outcomes of esophageal and gastric bone FBs in dogs - Retrospective study - 129 dogs (45 esophageal FB, 84 gastric FB) - Dogs with esophageal FB weighed slightly less and were significantly younger than with gastric FB - No difference in the calculated cross-sectional areas of gastric and esophageal FBs - Bone to body weight index (B : BWI) was significantly higher in dogs with esophageal vs gastric FB - B: BWI was significantly higher in dogs with FB entrapped in the middle or distal esophagus vs proximal esophagus - 40/45 dogs with EFB had clinical signs on presentation (gagging, vomiting, regurgitation, inappetence, retching, respiratory distress, coughing, hard swallowing, ptyalism, reverse sneezing); other 5 presented after witnessed ingestion - 100% had attempted endoscopy - successful in 42/45; 3/45 needed surgical removal after failing endoscopy - 9/42 cases had the bone pushed into the stomach - Adverse outcomes in 8/26 with available follow-up info, of which 2 strictures and 2 euthanasia - 62% has mucosal erosions (more erosions associated with increased chronicity and more distal entrapment) - PEG was not placed in any dogs who had the obstruction resolved non-surgically - 6 dogs had the bone left in the stomach for digestion without reported complications - FB had moved into the stomach in 3 cases before endoscopy (supposedly following muscle relaxation induced by GA) - 24/84 GFB had clinical signs on presentation (vomiting predominant sign in 83% of cases, anorexia, diarrhea, hypersalivation, abdominal distension) - 74% did not undergo intervention and the bone was left in situ for digestion (9 of these dogs had clinical signs on presentation) - Endoscopic removal attempted in 26% and successful in 91% (no complications reported) - Medications administered: omeprazole, famotidine, sucralfate, maropitant, ondansetron, metronidazole - Follow-up radiographs in 7 dogs only: FB resolved in 1 day in 2 dogs, and reduced in size on day 1 in another 3 dogs. In the other 2 dogs, the FB had resolved on repeated radiograph on day 14 and 18 - No evidence of short- or long-term complications in any case - B : BWI was significantly higher in dogs that underwent endoscopy vs conservative management - Endoscopic removal was more likely to be attempted in dogs with clinical signs and in dogs with larger B:BWI; endoscopy was less likely in older dogs **Beer et al, JAVMA 2022** - complications associated with and outcome of surgical intervention for treatment of esophageal FB in dogs (63 dogs) - 85.7% underwent surgery after unsuccessful minimally invasive procedure or due to evidence of esophageal perforation - Perforation was present at the time of surgery in 66.7% - Left cranial thoracotomy in 58.7% - Complications: - Intraoperative in 28.6% - Postoperative in 50% (3 dogs had dehiscence of esophagotomy site) - Survival to discharge: 74.6% - Negative prognostic indicators: esophageal perforation preoperatively, undergoing a thoracotomy, if gastrotomy tube was placed - Long-term infrequent vomiting or regurgitation in 25% [[Bongard et al, JVECC 2019]](https://onlinelibrary.wiley.com/doi/epdf/10.1111/vec.12875) - factors associated with degree of esophagitis, treatment and outcomes in dogs with esophageal FB (114 dogs) - Overall endoscopy success rate was 95% - Complication rate of 22% - Small breeds were overrepresented - Dogs with FB for \>24h were more likely to have severe esophagitis and major complications - FB type did not predict the degree of esophagitis or complications - BUT fish hooks were more likely to require surgical removal - Feeding tube were placed in 14% of dogs (15/16 gastrotomy tubes) and were more likely if FB had been present for \>24h [[Teh et al, JVECC 2018]](https://onlinelibrary.wiley.com/doi/epdf/10.1111/vec.12757) - medical management of esophageal perforation secondary to esophageal FB in 5 dogs - Pleural effusion seen on radiography prior to attempted endoscopy - Treatment provided: IVFT, IV antimicrobials, analgesia, proton pump inhibitors - 2/5 dogs had PEG tube placed - Complications after FB removal: pneumothorax (2/5) and pneumomediastinum (4/5) - 4/5 dogs survived to discharge; 1 was euthanized as a result of aspiration pneumonia following FB removal **Brisson et al, JAVMA 2018** - risk factors and prognostic indicators for surgical outcome in dogs with esophageal FB (233 dogs) - Terrier breeds were most common (30.5%) - Need for surgical intervention was associated with FB entrapment, body weight, anorexia, lethargy, rectal temperature, esophageal perforation - Poorer prognosis in older dogs, longer duration of FB entrapment and perforation - Endoscopic retrieval/advancement in the stomach was successful in 83.6% - Postprocedural strictures in 11.2% - Median duration of hospitalization: 1 day (need for surgery associated with longer hospitalization) - Overall mortality rate: 5.4% **Sterman et al, JAVMA 2018** - Likelihood and outcome of esophageal perforation secondary to esophageal FB in dogs (125 dogs) - Most common types of foreign bodies: bones (44%) and fish hooks (30%) - Esophageal perforation in 12% of cases - No association with body weight - More likely in dogs with fish hooks vs other FBs - Longer time between ingestion and initial evaluation in dogs with perforation - 87% of dogs with esophageal perforation survived to discharge - 8/15 survivors required [no surgical intervention] [[Burton et al, JVIM 2017]](https://onlinelibrary.wiley.com/doi/epdf/10.1111/jvim.14849) - risk factors for death in dogs treated for esophageal FB obstruction (222 dogs) - Bone foreign bodies most common (81%) - Distal esophagus most common location (49.5%) - Duration of clinical signs was NOT associated with risk of death - Entrapment was treated with endoscopy in 91.8% and surgery after endoscopy attempt in 5.9% - In-hospital mortality rate was 5% - Risk of death was significantly higher with surgery (OR 20.1) and 100% of dogs undergoing endoscopy died after surgery was recommended but declined; increased number of postprocedural complications (OR 3.44), esophageal perforation (OR 65.47) and post procedure esophageal hemorrhage (OR 11.81) - Esophageal stricture reported in 2.1% of survivors [[Thompson et al, JVECC 2012]](https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1476-4431.2011.00700.x) - retrospective study in 34 dogs - Most common FB were bone (29.7%) and rawhides (29.7%) - Median duration of clinical signs prior to presentation: 2.75 h - Most common location: caudal esophagus (59.3%) - Endoscopy successful in 33/33 cases -\> 9 FB were pulled out, 24 were pushed into the stomach - Esophagitis found in 28 dogs (82%) - mild in 14, moderate in 9 and severe in 4 - Dogs with longer duration of clinical signs and longer anesthesia were more likely to have moderate or severe esophagitis - Median LOH: 19h - Dogs with longer duration of clinical signs, FB in the caudal esophagus and moderate/severe esophagitis had longer LOH - No dogs experienced long-term complications - Complication rate was 82.5% (8 patients having more than 1 complications) - Esophagitis, aspiration pneumonia, pneumothorax **Giannella et al, JSAP 2009** - esophageal and gastric endoscopic FB removal (102 dogs) **Leib and Sartor, JAVMA 2008** - esophageal FB obstruction by dental chew treat in 31 dogs - Mainly in small dogs (83.9%) - Obstructions most commonly in distal esophagus (74.2%) - Esophageal lesions were moderate or severe in 86.7% of dogs - Most FB were pushed in the stomach (oral removal in only 25.8%) - Thoracotomy was necessary in 6 dogs - Esophageal strictures developed in 24% that survived - Overall mortality was 25.8% [[Rousseau et al, JVECC 2007]](https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1476-4431.2007.00227.x) - incidence of esophagitis following esophageal FB removal in dogs (60 cases) - Dogs with moderate-to-severe esophagitis had - Longer duration of clinical signs - Were more likely to present for lethargy, regurgitation/vomiting - Had longer recovery time - Greater morbidity (esophageal stricture, perforation, necrosis, diverticulum formation, aspiration pneumonia, pneumothorax, severe tracheal compression and death) - Dogs with mild esophagitis were more likely to present for gagging - Overall, dogs with moderate-to-severe esophagitis had significantly more complications than dogs with mild esophagitis **Sale et al, JAAHA 2006** - transthoracic esophagotomy FB retrieval in dogs (14 cases) - Successful in 13/14 dogs - Post-op complications in 2 dogs - pyothorax and SC edema - Overall recovery rate 93% **[Gastroesophageal intussusception (GEI)]** ![](media/image10.png) [[Brincin et al, JSAP 2022]](https://onlinelibrary.wiley.com/doi/epdf/10.1111/jsap.13395) - GEI secondary to emesis and subsequent septic pericardial effusion in a dog - GEI after induction of emesis with apomorphine - GEI manually reduced through diaphragmotomy **Grimes et al, JAVMA 2020** - characteristics and long-term outcomes of dogs with GEI (36 dogs) - Median age 13.2 months - Male 72% - GSD 33% - Most common clinical signs: vomiting (67%), regurgitation (33%) - 28% dogs euthanized with no treatment, 72% had treatment (25 surgically, 1 endoscopically) - 88% of treated dogs survived to discharge (MST 995 days) - 7/10 dogs had persistent regurgitation (improved with feeding strategy) - Dogs with acute clinical signs or previous diagnosis of megaesophagus were more likely to have persistent regurgitation **Martinez et al, JAAHA 2001** - intermittent GEI in a cat with idiopathic megaesophagus - GEI manually reduced by use of a stomach tube - Incisional gastropexy performed to prevent recurrence **[Gastroesophageal reflux (GER)]** GER in brachycephalic is suspected to be secondary to the high negative intrathoracic pressure to overcome the upper respiratory tract obstruction +/- sliding hiatal hernia +/- esophageal hiatus rim malformation - Dogs with substantial reflux may benefit from esophageal hiatal rim reconstruction Tue 1. \"equerry md nnure Oe Nature Of the respiratory signs Snoring Inspiratory efforts Stress or exercise intolerance Syncope Frequency Ne ver Occasionally once monthly) Regularly (once weekly) Grade 3 Daily (once daily) Often ( \> once daily) Constantly The grading Of the respiratory disorders ig based the frequency Of different Clinical gigng ig Corn%iged Of three gradeg\_ Inclusion Of at least one Sign in a higher determines the actual Classification. For example. if an animal was presented with regular difficulty. or but occasional a 3 for respiratory Signs wag assigned 2. \"equerry md nnure Nature of the digestive signs Ptyalism Regurgitation Vomiting Frequency Ne ver Occasionally once monthly) Grade 1 Regularly (once weekly) Daily (once daily) Often ( \> once daily) Constantly The grading Of the digestive disorders ig on the fregueru:y Of different Clinical Signs and ig Of three Inclusion Of at least Sign in a higher the actual Claggification. For if an animal wag presented With regular ptyåigm and regurgitation but daily a grade 3 for digestive Signs was assigned [[Poncet et al, JSAP 2005]](https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1748-5827.2005.tb00320.x) - in brachycephalic dogs [[Appelgrein et al, JVIM 2022]](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9151495/pdf/JVIM-36-927.pdf) - quantification of GER in brachycephalic dogs (51 dogs) - Esophageal probe with 2 pH sensors (proximal and distal) placed through the nose for 18-24 h in brachycephalic dogs presented for URT assessment - Proximal and distal reflux were identified by detection of fluid with a pH \ - [Prognosis]: mortality rate of 64% in dogs **[Chronic gastritis]** - [Prevalence]: 35% of dogs with chronic vomiting (26 to 48% of asymptomatic dogs); prevalence not determined in cats - [Causes]: underlying cause is rarely identified - Dietary allergy or intolerance - Occult parasitism - Reaction to bacterial antigens - Systemic disease - Ulcerogenic or irritant drugs - Parasites (Physaloptera, Ollulanus) - Fungal infections (Pythium insidiosum, Histoplasma) (rare) - [Pathogenesis]: complex interplay between GI microflora, epithelium, immune effector cells (e.g. lymphocytes, macrophages) and soluble mediators (e.g. chemokines, cytokines) - Inflammation may be the result of loss of tolerance to indigenous GI microflora or dietary antigens - Gram -ve or pathogenic bacteria induce proinflammatory cytokine (IL-8, IL-1-beta) secretion from epithelial cells - Commensal bacteria or other bacteria (e.g. Streptococcus faecium, Lactobacillus) induce production of immunomodulatory cytokines (TGF-beta, IL-10) - IL-10 modulates the production of proinflammatory cytokines - H pylori causes an infiltration of polymorphonuclear and mononuclear cells and upregulation of proinflammatory cytokines and chemokine IL-8, with production of IFN-gamma, IL-4 and IL-5 (Th1 type response) - [Clinical signs]: - Vomiting (food or bile) - Decreased appetite - Weight loss - Melena - Hematemesis - Dermatological signs - [Breed association]: - Basenjis: hypertrophy of fundic mucosa associated with severe gastritis - Drentse Patrijshonds: hypertrophy of fundic mucosa associated with stomatocytosis, hemolytic anemia, icterus, polyneuropathy - Small brachycephalic breed (e.g. Lhasa Apso): hypertrophy of pyloric mucosa associated with gastric outflow obstruction - Lundehunds with PLE: atrophy of gastric mucosa that may progress to adenocarcinoma - Young, large-breed male dogs in the US: granulomatous gastritis causes by Pythium (++ fall, winter and spring) - [Diagnosis]: - Serology for Pythium insidiousum - Food-specific IgE not useful - Gastric fluid cytology (Helicobater, parasite ova or larvae) - Impression smears of gastric biopsy (Helicobacter) - Biopsy urease test (Helicobacter) - Serum gastrin - Gastric histopathology - usually 3 biopsies from each region (pylorus, fundus and cardia) - Full thickness biopsy often required to differentiate gastritis from neoplasia or fungal infection - Predominant cellular infiltrate: eosinophilic, lymphocytic, plasmocytic, granulomatous, lymphoid follicular - Most common form in dogs is the superficial lymphoplasmacytic gastritis with concomitant lymphoid follicle hyperplasia - Presence of architectural abnormalities: atrophy, hypertrophy, fibrosis, edema, ulceration, metaplasia - Lesion severity: mild, moderate, severe - Dribbling dietary antigens on the gastric mucosa during endoscopy - to check for presence of food allergy (not useful in dogs and cats) - Highly subjective, detects only immediate hypersensitivity and does not correlate with dietary elimination trials Cellular - [Treatment]: - Detect and treat underlying metabolic disorders and remove drugs, toxins, FBs, parasites and fugal infections **[Parasitic gastritis]** - ***Ollulanus tricuspis***: microscopic worm (0.7-1 mm long, 0.04 mm wide) that infects feline stomach - Cat-to-cat transmission through ingestion of vomit + internal autoinfection - Mucosa abnormalities: none to rugal hyperplasia and nodular gastritis - Histopathology: lymphoplasmacytic infiltrates, lymphoid follicular hyperplasia, fibrosis - NOT detected by fecal examination - need evaluation of gastric juice, vomit or histologic sections - Treatment: fenbendazole 10 mg/kg PO SID for 2 days - ***Physaloptera spp***: 2-6 cm long worms that can be found in the stomach of cats and dogs (mainly parasites of coyotes) - Intermediate hosts: cockroaches, beetles; paratenic hosts: lizards, hedgehogs - Eggs burden in the feces is usually low and difficult to see on flotation as transparent - Treatment: pyrantel pamoate 5 mg/kg PO (1 dose in dogs, 2 doses in cats 14 days apart) - ***Gnathostoma spp*** (cats), ***Spirocerca spp*** (dogs), ***Aonchotheca spp*** (cats) - Cause gastric nodules that need to be surgically resected **[Gastric pythiosis]** (*Pythium insidiosum*) - [Definition]: causes transmural thickening of the gastric outflow tract with pyogranulomatous inflammation - [Diagnosis]: - Special staining (Gomori\'s methamine silver) - Culture - Serology - PCR of infected tissues - [Treatment]: for 2-3 months post-surgery - Itraconazole 10 mg/kg PO SID - Terbinafine 5-10 mg/kg PO SID - [Prognosis]: poor (\ - [Clinical signs]: - Vomit of food 6-10 hours after ingestion (could be projectile) - Abdominal distension - Weight loss - Melena - Abdominal discomfort - Anorexia - [Treatment]: - Diet: small amounts of semiliquid, protein and fat-restricted diets, fed at frequent intervals to facilitate emptying - Prokinetics - Not recommended to combine cisapride to erythromycin (possible adverse interactions) - Metoclopramide has prokinetic activity in stomach and upper GI tract + central antiemetic properties - Less effective for promoting gastroduodenal and intestinal motility than cisapride - Cisapride has no central antiemetic effects, it is more potent in promoting gastric emptying of solids than metoclopramide and has more drug interactions - Erythromycin releases motilin, acts on motilin receptors and mimics phase III of the interdigestive migrating myoelectric complex, promoting the emptying of solids - Ranitidine has prokinetic activity due to organophosphate-like effect **[Gastric neoplasia]** - \ myocardial ischemia - Cardiac troponins have been proved to be elevated in dogs with GDV and associated with severity of ECG changes and outcome - Circulatory cardiostimulatory (epinephrine) and cardioinhibitory (TNF-alpha, IL-1beta) substances - [Respiratory compromise if multifactorial] - Decreased total thoracic volume and normal caudal diaphragmatic excursion caused by gastric distension and increased intra-abdominal pressure -\> partial lung lobe collapse and decreased TV and ventilation-perfusion (V/Q) mismatching - RR and RE increase to compensate, but may be inadequate -\> hypercapnia and hypoxemia - Aspiration pneumonia (++ post-operative, and contributes to mortality) - Evidence of aspiration pneumonia in 14% of dogs with GDV preoperatively - [Gastrointestinal compromise] - Gastric necrosis (associated with increased morbidity and mortality) - decreased gastric blood flow due to a combination of factors - Compression - Thrombosis - Avulsion of splenic and/or short gastric arteries - Elevated intragastric pressure (gastric wall tension exceeds driving pressure in the gastric wall arterioles and capillaries) - Reduced cardiac output - Intestinal blood flow compromise -\> intestinal villous injury and mucosal barrier compromise, with translocation and increased circulating concentration of bacterial lipopolysaccharide -\> systemic inflammation + can contribute to post-op ileus (in association with GA and analgesic drugs) - Direct compression of portal vein - Decreased cardiac output - Haemoabdomen due to rupture of the short gastric arteries - [Splenic compromise] (associated with worse outcome) - Splenic vascular avulsion - Intravascular thrombosis - Splenic torsion - Splenic infarction - [Acid-base status abnormalities] - High anion gap (lactate) metabolic acidosis (due to low DO2) - Hypochloremic metabolic alkalosis (sequestration of gastric HCl acid) - Respiratory acidosis (dye to hypoventilation and hypocapnia) - [Electrolytes abnormalities] - Hypokalemia (due to administration of large volume of low-potassium fluids, sequestration within the stomach, loss through vomiting or lavage, transcellular shifting if hypochloremic metabolic alkalosis, activation of RAAS system, catecholamine-induced intracellular shifting) - [Disseminated intravascular coagulopathy (DIC)] due to - Pooling of blood in the caudal vena cava, portal vein or splanchnic circulation - Tissue hypoxia - Acidosis - Systemic inflammation - Endotoxemia - +/- sepsis - [AKI] - Detected by creatinine-based criteria in 2.3% and 8% of dogs with GDV ([Bruchim et al, JVECC 2012; Buber et al, JAVMA 2007]) - Risk factor for mortality [Consequences of GDV]: - Impaired gastric blood supply - Obstructive and distributive shock - Decreased systemic tissue perfusion and ischemia **Epidemiology** - Large and giant breeds ++, but small breeds and cats can be affected too - Breeds: Great Dane, Weimaraner, Saint Bernard, Gordon Setter, Irish Setter, Standard Poodle, GSD - Adult dogs - Older age dogs are at higher risk - Risk factors (genetic and environmental): - First-degree relatives that have had GDV (genetic predisposition) - Higher thoracic depth-to-width ratio - Lean body condition - Advancing age - Large drop of environmental T° over a short period of time - Eating quickly (in large but no in giant breed dogs) - Stressful events (e.g. boarding, traveling, vet visit) - Fearful, nervous or aggressive temperament - Diet-related factors (e.g. raised food bowl, being fed only dry food, small kibble size, single large meal/day) - Post-prandial exercise (not found as risk factor in more recent study - actually beneficial?) - Failure of normal eructation - Anesthesia - Aerophagia - Pyloric outflow mechanisms (e.g. laxity or agenesis of perigastric ligaments - causative or consequence of GDV?, or due to splenic masses or torsion and splenectomy \[more recent studies failed to confirm this association\]) - Gastric FBs (in at-risk breeds) **Clinical signs** Acute onset - Restlessness, anxiety - Hypersalivation - Unproductive retching and/or vomit attempts - Collapse - Distended, bloated abdomen Physical examination: depressed mentation, pale MM, prolonged CRT, tachycardia, weak pulses, +/- irregular cardiac rhythm and pulse deficit; increase RR and RE; abdomen distended and firm on palpation, tympanic; splenomegaly and spleen displaced caudally **Diagnosis** - Single (RIGHT) lateral abdominal radiograph - GDV: Pylorus moves cranially and dorsally from the gastric fundus from which is separated by a soft tissue opacity (**reverse C**, **double bubble** or **Popeye sign**) - GD: pylorus lies ventral to the fundus ![](media/image18.png) - +/- DV or VD (if unclear gastric position on the lateral) - GDV: pylorus is to the left of the midline - GD: pylorus is to the right of the midline - Gastric necrosis on radiographs - Pneumatosis (intramural gas) and pneumoperitoneum suggest possible perforation - Thoracic radiographs - to detect aspiration pneumonia or metastatic disease in older dogs - Minimum database: PCV, TS, lactate - Initial plasma lactate \40% reduction in plasma lactate following fluid resuscitation are associated with increased survival and fewer complications - Initial lactate \>6 mmol/L may be associated with gastric wall necrosis and increased cost of care - Failure of hyperlactatemia to improve with stabilization is a predictor of non-survival in dogs with GDV - CBC: thrombocytopenia due to PLT consumption or DIC - Presence of DIC correlates with gastric necrosis and is a negative prognostic indicator for survival - Biochem: increased hepatic transaminase (hepatocellular damage) and/or azotemia (generally prerenal) **Treatment** - Goals: - Improve cardiovascular status - Flow-by oxygen - Multiple large bore IV catheters - Large volumes of isotonic crystalloids +/- hypertonic saline (obstructive component of shock cannot be resolved until the volvulus is corrected) - Analgesia (full mu-agonist opioid) - +/- Vasopressors - +/- Lidocaine - Antibiotics (IF aspiration pneumonia or gastric perforation or neutropenia) - Gastric decompression - Orogastric intubation - Rapid induction of GA with opioid analgesia and intubation - Mark tube from nares to caudal edge of the last rib - Lubricate tube - Trocar insertion (if orogastric tube does not pass easily) - Clip and aseptically prepare - Large-gauge, short needle or over-the-needle catheter (14 or 16G) in a region of the left or right cranial, dorsolateral abdomen (area which exhibits the greatest tympany) - Successful placement is confirmed by a hissing sound as gas is released from the distended stomach (or guide with AUS) - Gentle compression of the abdominal wall opposite the site of the catheter may aid in maximizing decompression - Repositioning and pexy of the stomach - [Lidocaine] - Properties - Potent local anesthetic - Class Ib antiarrhythmic - Scavenger of reactive O2 species - Inflammatory modulator - Reported cardio- and gastroprotective properties and reduced gastric tissue damage in dogs with experimentally induced GD ([Pfeiffer et al, Acta Physiol Hung 2006]) - Decreased incidence of AKI and cardiac arrhythmias and length of hospitalization in dogs with GDV receiving lidocaine CRI over 24h ([Bruchim et al, JVECC 2012]) 1. ***GD*** - IVFT - Orogastric intubation - Simethicone (2-4 mg/kg PO q6h) - Metoclopramide (0.2-0.4 mg/kg SC q8h) - Gastropexy (to prevent GDV in the future) - Surgical exploration if not responsive to medical management 1. ***GDV*** (surgical treatment) - Goals - Decompress and reposition the stomach - Assess viability of stomach and spleen and remove irreversible compromised tissue - Create permanent adhesion between stomach and body wall (to prevent relapse) - Technique of [repositioning] - Large ventral midline incision (pulling up the linea alba to avoid damage of underlying viscera) - The pylorus has normally moved from its normal position (on the right, next to the body wall) toward the left body wall, in a clockwise direction - Rotation may be 90 to 360 degrees (most commonly (180 to 270 degrees) - The greater omentum is found draped over the cranial abdominal organs - Decompress stomach by orogastric intubation (by the anesthetic with guidance of the surgeon) or via gastrocentesis - Stomach is rotated back into its normal position (the pylorus can be located by tracing the duodenum - attached to the pancreas) by gently bringing the pylorus back to the right of the midline using one hand and using the other hand to push the body of the stomach dorsally - Decompress stomach totally with orogastric tube at this stage - +/- gastrotomy if obstructive material is present within the gastric lumen - Assess stomach and spleen for viability (gastric resection and/or splenectomy performed as needed) - Spleen should be removed only if thrombosed or damages - Technique of [partial gastrectomy] (if gastric necrosis - gray or black coloration and palpable thinning of the stomach) - Preplace stay suture to minimize or prevent abdominal contamination - Resect devitalized area until bleeding tissue is reached OR invaginate necrotic tissue - Ideally less technically demanding and less likely to result in peritoneal contamination - BUT invaginated tissues are more prone to ulcer formation - Closure (suture or stapling \[TA-90 or GIA-50\]) with a second inverting suture - Technique of [gastropexy] - The pyloric antral region is fixed to the right body wall - Muscular flap - Circumcostal - Belt loop - Incisional: approx 5 cm incision made in the transversus abdominis muscle just caudal to the last rib and corresponding incision is made on the gastric seromuscular layer (take care NOT to enter in the gastric lumen) - Try to maintain a relatively normal gastric position when the 2 edges are sutured together (with polypropylene or polydioxanone 2-0) - The pexy site should not be incorporated in the abdominal closure (stomach could be damaged if a cranial abdominal surgery is required again in the future) - Gastrocolopexy - Ventral midline (incorporating gastropexy) - Consider GI biopsy for histopathology if previous history of chronic GI signs - Place NG tube (monitoring of GRV, removal of excessive gas/fluid, nutrition. **Postoperative care** - IVFT (at reasonably high rate for 48-72 h) - Monitoring: perfusion parameters, PCV, TS; urine output, ECG, blood pressure, acid-base balance and lactate - Food can be offered as soon as awake from anesthesia if the dog is stable - Antiemetic - Anti acids and gastric-coating agents may be considered - Cardia arrhythmias usually begin 12-24 h after surgery - continuous ECG - Treatment if - Reduced cardiac output and hemodynamic instability - R on T phenomenon - Multiform ventricular premature contractions - Sustained Vtac with HR \>180 bpm **Prognosis** - Mortality rate: 10-43% - Factors associated with increased survival - Rapid intervention - Reduction in lactate levels with treatment - Absence of gastric necrosis - Serum myoglobin level \

Gastrointestinal.docx

Document Details

Tags

Related

Full Transcript

Upgrade to continue