Is there an age at which the ductus venosus should be closed? With normal liver enzyme levels could a shunt be a cause of vomiting and lethargy? Is this look like a shunt. 10 Week male Briard woth episodes of lethargy, vomiting and weakness/ataxia.
Apparently ate a christmas ornament and is vomiting. Lab work WNL at present.
Is there an age at which the ductus venosus should be closed? With normal liver enzyme levels could a shunt be a cause of vomiting and lethargy? Is this look like a shunt. 10 Week male Briard woth episodes of lethargy, vomiting and weakness/ataxia.
Apparently ate a christmas ornament and is vomiting. Lab work WNL at present.
Comments
According to this old paper
According to this old paper the duct should close within the first week of life:
Oliveira MC, Pinto E Silva P, Orsi AM, Define RM. Anatomical observations about the closure of the ductus venosus in the dog (Canis familiaris). Anat Anz. 1979;145:353-8.
The observation of the anatomical closure of ductus venosus was carried out in 108 dogs (62 females and 46 males) with age varying between 3 hours and 21 days old. We have observed that within 2 days old, the ductus venosus was found pervious in 100% of the animals sacrified; 3 days old, in 81% of the animals; 4 days old, in 62% of pups; 5 days old, in 25% and over 6 days old, the ductus venosus was anatomical closed in 100% of the animals. We have also observed that the closure starts within 48 hours on the caudal vena cava caudal side.
The episodic signs of lethargy, vomiting, weakness/ataxia fit with a shunt but the pre-and post-prandial acids should then be elevated. Recent history is more typical for a GI foreign body or irritation; but may also have had too much high-protein Christmas food 🙂
Bile acids are pending. I
Bile acids are pending. I will post them when I get them Thanks for the info and the reply.
This is a beautiful IH shunt
This is a beautiful IH shunt & looked central divisional by the contour and positioning. Needs a vascular plug. Stateside the best at this that I know of is Chick Weiss at AMC.
Revision after seeing full case:
So I read this case out on telemed as well thx for sending and Dr Ondreka and I both looked at it and its actually a right divisional but the biggest looping right divisional IH shunt that I have seen. I attached some stills and arrows below. Really cool case and nice scan for sure. The one key image form the right intercostal approach about IC 11-12 Im gussing was key to seeing the connection of the right pv branch into this expanding shunt. From the clinical history sounds like this dog is in stage 3-4 hepatic encephalopathy potentially induced by the acute phase GI issues.
Here are some quick nerdy info from my ABVP exam notes on HE:
Hepatic encephalopathy:
Diff diagnosis
metabolic encephalopathy brain tumor CNS infection hemorrhage hydrocephalus epilepsy ischemia and toxins
Four stages:
Stage 1: mild confusion inappetence, dull
Stage 2: lethargy ataxia very dull head pressing blindness salivation
Stage 3: uncoordinated confused stupor in active but aroused severe salivation and seizures
Stage 4: recumbent unarousal, coma
Three categories of hepatic encephalopathy
Type A: acute liver failure: toxins infectious ischemia metabolic>SIRS acute cerebral Edema and intracranial hypertension
Type B: portosystemic shunting without liver disease
Type C: severe hepatic parenchymal disease and portal hypertension multiple acquired shunts
Types A & B respond to medical management
Brain neurotoxins: AGGBT ammonia glutamine GABA benzodiazepine, tryptophane
Ammonia Generation:
1: degradation of intestinal protein and urea by the colon/ urease producing bacteria
2: hepatic metabolism of dietary amino acids
3: enterocyte metabolism of glutamine
4: muscle catabolism
2 pathways:
Ammonia > urea > kidneys > urine
Ammonia > glutamine synthesis by tissues > intestinal mucosa and kidneys > ammonia recirculates
Ammonia (normally metabolized by the liver) accumulation occurs by PSS liver bypass, or diffuse liver dysfunction
Glutamine metabolized by astrocytes in the brain> overload> ammonia toxicity> reduced CNS glucose and oxygen metabolism and increased permeability to ammonia > Cns signs
GABA inhibitory neurotransmitter accumulates owing to liver dysfunction
Amino acid byproducts such as tryptophan tyrosine phenylalanine act as false neurotransmitters blocking catecholamine activation
Intracranial hypertension clinical signs type A:
Hypertension miosis D cerebral posture irregular respiration
CT for brain edema
CSF tap for glutamine glutamate aromatic amino acids elevation
MRI for PSS
Point of care ammonia tests have false-negative results
Blood ammonia elevates when liver failure exceeds 70% of decreased urea cycle function and secondary PSS occur
Protein C is < 70% in PSS
> 70% with portal vein hypoplasia
Acute phase disease stimulated by Gastrointestinal hemorrhage excessive protein intake infection metabolic derangements renal failure and dehydration
Increased protein load stimulates ammonia bacteria release and GABA. Both serve as Neurotoxins and result in poor hepatic function
Ornithine and aspartate TX HE by converting ammonia to urea and glutamine
Predisposition to infection going to reduced leukocyte migration bacterial activity in paired phagocytosis and malnutrition secondary SIRS
Non ionized ammonium exacerbates HE> alkaline urine
HE treatment: gi protect, fluid support, avoid diazepam and other sedatives,
Mannitol for Cns edema 0.5-1.5 mg/kg over 15 min
Levetiracetam for seizures 20 mg/kg Iv q 8 hrs
Plant based high qual. protein. Not red meat Fish eggs result in the high ammonium creation.
Lactulose 1-3 ml/ 10 kg tid target 2-3 soft stools/day
Metronidazole 7.5 mg/kg bid/tid
Zinc 1-3 mg elemental zinc/kg/ day zinc acetate target serum zinc 200-500 ug/dl
Tx 72 hours if no improvement for HE then look for other factors
Merry Xmas to all:)… Here
Merry Xmas to all:)… Here is an excerpt from the Curbside Guide now avaialble for purchase and immediate download and hard copy prepurchase for Jan 15.
http://www.sonopath.com/curbside-guide-combo-pack-ebook-and-softcover-now-available-purchase
This is the elevated bile acid/shunt chapter without the images but with the member link of the chapter to related cases
Bile Acid Elevations and Hepatic Vascular Disorders:
Portosystemic Shunts and Portal Vein Hypoplasia (Microvascular Dysplasia)
http://www.sonopath.com/BAShunts
Non-Shunt Pathologies and Elevated Bile Acid Levels
Description: Bile acids are conjugated with cholesterol in the liver; they then enter the biliary tree and are stored in the gallbladder. Under the stimulation of cholecystokinin, the gallbladder contracts and bile acids are released from the cystic duct into the common bile duct; they then pass through the sphincter of Oddi to reach the duodenum. Bile acids are absorbed primarily in the ileum (95%), and then reenter the portal system and move into the liver. This enterohepatic circulation cycle can occur 2-5 times within the space of a single meal. When bile flow is obstructed and the bile secretory pressure reaches 30 cm H20, bile acids accumulate in the blood. Obstruction can occur due to calculi, the accumulation of acids (also known as “bile sludge”) in the common bile duct, or extrahepatic obstruction, such as pancreatitis. Unconjugatedbile acids are cytotoxic and result in inflammation, intestinal necrosis, poor permeability, bacterialtranslocation, sepsis, endotoxemia, poor micelle formation, and a deficiency of fat-soluble vitamins.
Causes of Bile Acid Elevation:
1. Nonhepatic Causes
2. Hepatic Causes
Hepatic Vascular Diseases
Description: Hepatic vascular diseases can be divided into congenital and acquired forms. Congenital disorders include: portosystemic shunting (PSS) or portosystemic vascular anomalies (PSVA), both intrahepatic (IHPSS) and extrahepatic (EHPSS); microhepatic PSS, also called portal vein hypoplasia (PVH) (previously known as microvascular dysplasia [MVD]) without portal hypertension; portal vein atresia; and hepatic arteriovenous (AV) malformations. Acquired forms include: acquired shunting secondary to portal hypertension due to primary hepatic disease; fibrosis/cirrhosis; and non-cirrhotic portal hypertension. Although PSVA can result in elevated liver enzymes and bile acids, other possible causes for elevated bile acids include, but are not limited to: diffuse hepatocellular disease; cholestatic disease; cholecystectomy; spontaneous gallbladder contraction; ursodeoxycholic acid use; inflammatory bowel disease; hyperlipidemia; prolonged anorexia; hyperadrenocorticism; pancreatitis; severe ileal disease or resection; delayed gastric emptying; prolonged or rapid intestinal transit time; small intestinal bacterial overgrowth; and breed-associated increases, as observed in the Maltese breed, for example, in the absence of primary hepatic disease. Given the long list of differentials, the assessment for PSVA often depends on the clinical presentation, such as signalment, clinical signs, and specific laboratory findings, which may suggest PSVA. Ultrasound and additional diagnostics are imperative in the diagnostic process.
The following canine breeds—typically small breed dogs—are predisposed to congenital extrahepatic shunting: Miniature Schnauzer, Yorkshire Terrier, Pug, Dachshund, Cairn Terrier, Shih Tzu, West Highland White Terrier, Bichon Frisé, Havanese, Dandie Dinmonts, and Maltese. Extrahepatic shunts often involve a shunt from the portal vein (PV), left gastric, or splenic vein, to the caudal vena cava. The shunt may occasionally enter the azygous vein dorsally, bypassing the vena cava (VC). The following breeds—typically large breed dogs—are predisposed to intrahepatic shunting: Irish Wolfhound, Australian Cattle Dog, Australian Shepherd, Golden Retriever, Old English Sheepdog, and Labrador Retriever. Intrahepatic shunting in the latter breeds most commonly presents as a shunt between the PV and the caudal vena cava, and may coexist with PVH. Yorkshire Terriers and Cairn Terriers are predisposed to PVH.
PVSA are not seen as commonly in cats compared to dogs. In cats, extrahepatic PSVA usually arise from the left gastric vein; they also often have a patent ductus venosus. The following feline breeds are predisposed to PVSA: domestic shorthair, Persian, Siamese, Himalayan, and Burman.
Clinical Signs: Dogs affected with PVH uniquely are typically asymptomatic and their hepatic vascular abnormalities are non-progressive; however, patients with severe PVH may sometimes display clinical signs similar to those with PSVA.
A patient with PSVA is often more symptomatic; clinical findings vary. Dogs and cats with PSVA often have smaller bodies compared to their litter mates, and may exhibit anorexia, vomiting, diarrhea, depression, lethargy, ataxia, head pressing, “stargazing,” behavioral changes, seizures, and/or coma. Drooling is common in cats, but can be seen in dogs as well. Renomegaly is common in patients with PSVA, and polyuria and polydipsia (PU/PD) can occur due to low BUN in the face of hepatic insufficiency. Signs of lower urinary tract disease manifest if urate calculi have formed. Animals with PSVA also have an increased susceptibility to infections due to reduced Kupffer cell function. Minor bite wounds, tick bites, subcutaneous infections, lacerations, and even vaccinations may cause illness that can require hospitalization. Cats with PSVA may have copper-colored irises (36%). Dogs with portoazygous shunts are generally the least symptomatic and frequently present with ammonium biurate calculi as adults; their disorder is often discovered serendipitously. Generally, asymptomatic dogs (15-20%) whose PSVA is only detected later in life usually respond well to PSVA ligation. Acquired shunting may occur later in life secondary to chronic hepatic disease and can result in portal hypertension and ascites.
Diagnostics: Clinicopathologic findings for both PSVA and PVH may include mild hypoalbuminemia, hypoglycemia, hypocholesterolemia, microcytosis (low MCV), and hypochromasia. One may also note the following: borderline, non-regenerative anemia; target cells; low BUN; low creatinine; normal to variable increases in liver enzymes (mild to modest); and ammonium biurate crystalluria (a minimum of 3 urine specimens should be examined). Radiographic findings may include microhepatica in dogs; however, liver size is variable in cats, and kidneys may be large in both species. Contrast portography yields varying patterns in patients with PSVA. Fasting plasma ammonium determination is more sensitive than bile acid profiles when gauging the presence of either congenital or acquired shunting; however, ammonium levels must be measured immediately upon collecting blood in a lithium heparin tube. The ammonium tolerance test or baseline ammonium level measurement is not practical if in-house testing is not available. Most dogs with PSVA have postprandial bile acid concentrations greater than 100 nmol/L, but values do not correlate with the severity of the disease. Dogs with PSVA have lower clotting factor activity than healthy dogs; this can cause complications during surgery. Protein C is an anti-thrombotic protein that is synthesized in the liver; it is used as a hepatic function test in people and is a better indicator of portal venous flow than total serum bile acids. In combination with serum bile acids, it can help differentiate PSVA from PVH, as dogs with PVH will have more normal protein C levels than those with PSVA. Markedly low levels of protein C suggest that a patient is likely a poor candidate for surgical ligation and also help identify dogs with hepatic failure.
Treatment: The majority of dogs affected with PVH alone do not require medical treatment and have a normal life expectancy. The severity of clinical signs in symptomatic PSVA patients is highly variable and can be regulated in large part by an appropriately formulated low-protein diet. Surgical treatment for PSVA is the subject of much debate; however, a recent study confirmed that long-term survivability was improved by surgical correction. Medical management remains a reasonable alternative. If surgery is to be pursued, it should be considered in light of comorbidities that influence hepatic integrity. Extrahepatic shunts are more accessible and therefore more amenable to ameroid ring constriction or shunt ligation, while intrahepatic shunts are often difficult to access surgically, as they are positioned deep within the liver parenchyma but may be closed with coil embolization under fluoroscopic guidance. Other considerations include whether the patient should be stabilized medically before surgery is attempted or if full recovery is to be expected once the PSVA is closed. The most common and severe complications of surgical ligation include portal hypertension and ascites, which is why slow attenuation via ameroid ring placement is often preferred, as well as the development of seizures/status epilepticus. Seizure development cannot always be predicted and is more common in small breed dogs, especially Maltese, and in cats.
The medical management of PSVA primarily involves restricting dietary protein (2.2-2.5 g/kg/day of protein, administered in small, frequent meals). Protein sources such as dairy, soy, and egg are enriched in branched-chain amino acids, which bypass liver metabolism and help reduce blood ammonia levels. Unsuccessful medical management is determined by recurrent hepatic encephalopathy or persistent ammonium biurate crystalluria. In both cases, if the animal has PSVA, one should consider surgical intervention or additional medical therapy. Lactulose should be started at a low dose (0.25 ml-1 ml/kg BID-TID) and titrated to achieve several soft stools per day. It acidifies the pH in the colon, which reduces urease activity and reduces urease-producing bacteria. Antibiotics, such as metronidazole (7.5 mg/kg PO BID) and neomycin (22 mg/kg PO BID), are utilized to modify enteric flora and reduce toxin production from urease-producing bacteria. Dogs with unresponsive hepatic encephalopathy are also managed with retention enemas (5-10 ml/kg with 20% lactulose), which rapidly acidify colonic contents.
Conclusion: PSVA and PVH are not uncommon in veterinary medicine. Medical therapy as well as surgical correction must be considered carefully in light of clinical presentation and shunt location. In all cases, dietary modification is the first-line treatment of choice; however, mild cases of PVH may not even require diet change.
References:
Allen L, Stobie D, et al. Clinicopathologic features of dogs with hepatic microvascular dysplasia with and without portosystemic shunts: 42 cases (1991-1996). J Am Vet Med Assoc 1999;214:218-20.
Christiansen JS, Hottinger HA, Allen L, et al. Hepatic microvascular dysplasia in dogs: a retrospective study of 24 cases 91987-1995). J Am Anim Hosp Assoc 2000;36:385-89.
Gerrizen-Bruning MJ, van den Ingh TS, Rothuizen J. Diagnostic value of fasting plasma ammonia and bile acid concentrations in the identification of portosystemic shunting in dogs. J Vet Intern Med 2006;20:13-19.
Greenhalgh SN, Dunning MD, McKinley TJ, et al. Comparison of survival after surgical or medical treatment in dogs with a congenital portosystemic shunt. J Am Vet Med Assoc 2010;236:1215-20.
Hunt GB. Effect of breed anatomy of portosystemic shunts resulting from congenital diseases in dogs and cats: A review of 242 cases. Aust Vet J 2004;82:746-49.
Kummeling A, Teske E, Rothuizen J, et al. Coagulation profiles in dogs with congenital portosystemic shunts before and after surgical attenuation. J Vet Intern Med 2006;20:1319-26.
Lamb CR, Daniel GB. Diagnostic imaging of dogs with suspected portosystemic shunting. Compend Contin Educ Pract Vet 2002;24:626-35.
Schermerhorn T, Center Sa, Dykes NL et al. Characterization of hepatoportal microvascular dysplasia in a kindred of cairn terriers. J Vet Intern Med 1996;10;219-30.
Toulza O, Center S, Brooks M, et al. Evaluation of plasma protein C activity for detection of hepatobiliary disease and portosystemic shunting in dogs. J Am Vet Med Assoc 2006;229:1761-71.
Windsor RC, Olby NJ. Congenital portosystemic shunts in five mature dogs with neurological signs. J Am Anim Hosp Assoc 2007;43:322-31.