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Prospective studies of prenatally diagnosed fetus prior to 25 wk. Krill Oil Dosage The dosage for krill oil which is made from crustaceans rather than fish is mg per day. This is such an important topic that I have an entire page devoted to phosphorus control. Archived from the original on 10 July Please do not steal from me by taking credit for my work. Retrieved January 31,

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Correct dehydration, acid-base disturbances, respiratory distress and decompress proximal esophageal pouch Reploge tube. Delayed repair gastrostomy first for all other patients. Repair consists of muscle-sparing thoracotomy, closure of TEF and primary anastomosis. Esophagogram is done days after repair. Most important predictors of outcome: Increase survival is associated with improvements in perioperative care, meticulous surgical technique and aggressive treatment of associated anomalies.

More than H-type is N-type, due to the obliquity of the fistula from trachea carina or main bronchi to esophageal side see the figure anatomically at the level of the neck root C7-T1. Pressure changes between both structure can cause entrance of air into the esophagus, or esophageal content into the trachea. Thus, the clinical manifestation that we must be aware for early diagnosis are: Diagnosis is confirmed with a well-done esophagogram, or video-esophagogram high success rates, establish level of the TEF.

Barium in the trachea could be caused by aspiration during the procedure. Upon radiologic doubt bronchoscopy should be the next diagnostic step. Any delay in surgery is generally due to delay in diagnosis rather than delay in presentation. Management consists of surgical closure of the TEF through a right cervical approach. Working in the tracheo-esophageal groove can cause injury to the recurrent laryngeal nerve with vocal cord paralysis.

Recurrence after closure is rare. The three most common anastomotic complications are in order of frequency: Tension on the anastomoses followed by leakage may lead to local inflammation with breakage of both suture lines enhancing the chance of recurrent TEF. Once established, the fistula allows saliva and food into the trachea, hence clinical suspicion of this diagnosis arises with recurrent respiratory symptoms associated with feedings after repair of esophageal atresia.

Diagnosis is confirmed with cineradiography of the esophagus or bronchoscopy. A second thoracotomy is very hazardous, but has proved to be the most effective method to close the recurrent TEF.

Either a pleural or pericardial flap will effectively isolate the suture line. Pericardial flap is easier to mobilize, provides sufficient tissue to use and serves as template for ingrowth of new mucosa should leakage occur. Other alternatives are endoscopic diathermy obliteration, laser coagulation, or fibrin glue deposition. Congenital gastric outlet obstruction is extremely rare. It occurs either in the pyloric or antral region. They probably represent the developmental product of excess local endodermal proliferation and redundancy.

The diagnosis should rely on history, contrast roentgenology studies and endoscopic findings. Symptoms are those of recurrent non-bilious vomiting and vary according to the diameter of aperture of the membrane. There is a slight male predominance with fair distribution between age groups in children.

History of polyhydramnios in the mother. Demonstration of a radioluscent line perpendicular to the long axis of the antrum is diagnostic of a web. Endoscopy corroborates the diagnosis. Management can be either surgical or non-surgical. Surgical Tx is successful in symptomatic pt. Other alternative is endoscopic balloon dilatation or transection of the web. Non-obtructive webs found incidentally can be managed medically with small curd formula and antispasmodics. The presence of an abnormally dilated gastric bubble in prenatal sonography should alert the physician toward the diagnosis of congenital antro-pyloric obstruction.

Is an abnormality of the pyloric musculature hypertrophy causing gastric outlet obstruction in early infancy. The incidence is 3 per live births. The etiology is unknown, but pylorospasm to formula protein cause a work hypertrophy of the muscle. The treatment consist in correction of hypochloremic alkalosis and state of dehydration and performing a Fredet-Ramstedt modified pyloromyotomy. Post-operative management consist of: Occur distal or proximal to the ampulla of Vater.

Most commonly distal to ampulla and therefore bilious vomiting is present. Bilious vomiting is surgical until proven otherwise in a baby. The first major event in the differentiation of the duodenum, hepatobiliary tree, and pancreas occurs at about the third week in gestation, when the biliary and pancreatic buds form at the junction of the foregut and the midgut. The duodenum at this time is a solid cord of epithelium, which undergoes vacuolization followed by recanalization and restitution of the intestinal lumen over weeks of normal development.

Failure of recanalization of the second part of the duodenum results in congenital obstruction of the lumen, often in conjunction with developmental malformation of the pancreatic anlagen and the terminal part of the biliary tree.

In support of this concept is the high incidence of annular pancreas observed, believed to represent a persistence of the ventral pancreatic anlage in association with intrinsic duodenal obstruction. Congenital partial obstruction of the duodenum can be either intrinsic membrane, web or pure or extrinsic Ladd's bands, annular pancreas. This does not entail a higher risk of early mortality unless associated with cardiac malformations.

Other associated conditions are malrotation midgut volvulus is rare due to absent bowel distension and peristalsis , biliary tract anomalies and Meckel's diverticulum. The diagnosis is suggested in utero by the double-bubble image on ultrasound. Vomiting is the most frequent presenting symptom. UGIS is diagnostic, showing a dilated stomach and first duodenal portion with scanty passage of contrast material distally. Management varies accordingly to the type of stenosis: Ladd's bands are lysed.

Pure stenosis is opened longitudinally and closed transversely Heineke-Mickulicz. Membranous stenosis is resected. Successful endoscopic membranectomy of duodenal stenosis has been reported. Duodeno-duodenostomy is the procedure of choice for annular pancreas. Diaphragms can rarely be double.

Anastomotic malfunction requiring prolonged intravenous nutrition and hospitalization has prompted development of a diamond shape larger stoma. Tapering or plication of the dilated duodenum is another effective method of improving disturbed transit.

Other complications after surgery are megaduodenum with blind loop syndrome, biliary reflux, cholestatic jaundice, delayed transit and bowel obstruction. Early mortality is associated to prematurity and associated malformations. Long-term follow-up is warranted to identify late problems.

The diagnostic characteristics are: The rotation and normal fixation of the intestinal tract takes place within the first three months of fetal life. In the earliest stages when the intestinal tract is recognizable as a continuous tube, the stomach, small intestine, and colon constitute a single tube with its blood supply arising posteriorly.

The midgut portion of this tube, from the second portion of the duodenum to the mid-transverse colon, lengthens and migrates out into an extension of the abdomen, which lies at the base of the umbilical cord. Here this loop of bowel undergoes a degree counterclockwise twist at its neck.

In the center of the twisted loop lie the blood vessels that will become the superior mesenteric artery and vein. After rotation, the small intestine quite rapidly withdraws into the abdominal cavity, with the duodenum and the proximal jejunum going first.

During this process the duodenojejunal junction goes beneath and to the left of the base of the superior mesenteric vessels. This leaves the upper intestine, including the stomach and the duodenum, encircling the superior mesenteric vessels like a horseshoe with its opening on the left side of the embryo.

The small intestine then follows into the abdomen, and withdrawal of the right half of the colon takes place so that it lies to the left. At the next step, the cecum and the right colon begin to travel across the top of the superior mesenteric vessels and then down to the right lower quadrant. The colon now lies draped across the top of the superior mesenteric vessels, again like a horseshoe, with its opening placed inferiorly.

The duodenojejunal loop is said to attach to the posterior abdominal wall soon after its turn, whereas the mesenteric attachments of the entire colon and of the remaining small bowel gradually adhere after they arrive in their normal positions. In malrotation the right colon can create peritoneal attachments that include and obstruct the third portion of the duodenum Ladd's bands. The diagnostic hallmarks are: A UGIS is more reliable than barium enema, most patients present in first month of life neonatal , but may present at any time.

The treatment is immediate operation; volvulus often means strangulation. Needs fluid and electrolyte replacement. Ladd's procedure consist of: In cases of questionable non-viable bowel a second look procedure is required.

Meconium ileus is a neonatal intraluminal intestinal obstruction caused by inspissated meconium blocking the distal ileum. The meconium has a reduced water, abnormal high protein and mucoproteint content, the result of decreased pancreatic enzyme activity and prolonged small bowel intestinal transit time.

Meconium Ileus is classified into two types: The distal small bowel cm of distal ileum is relatively small, measuring less than 2 cm in diameter and contains concretions of gray, inspissated meconium with the consistency of thick glue or putty. It is often beaklike in appearance, conforming to the shape of the contained pellets. Proximally, the mid-ileum is large, measuring up to 7 cm in diameter. It is greatly distended by a mass of extremely thick, tenacious, dark green or tarry meconium.

The unused small colon microcolon contains a small amount of inspissated mucus or grayish meconium. A cystic mass or atresia of the bowel may occur. The degree of obstruction varies, may be cured in mild cases by rectal irrigations. Failure to pass meconium, abdominal distension and vomiting are seen in more severe cases. The diagnosis is suspected with findings of: Some cases may show calcifications in the peritoneum Meconium peritonitis.

This test is not useful in infant during first weeks of life. It consist of a careful gastrograffin enema after the baby is well-hydrated. Gastrograffin is a hyperosmolar aqueous solution of meglumine diatrizoate containing 0.

Long-term prognosis depends on the degree of severity and progression of cystic fibrosis pulmonary disease. Total colonic aganglionosis TCA is found in approx. There are three critical phases for patients with TCA The first period comprises the time from birth until correct diagnosis.

Patients with TCA present with a large variety of symptoms. Several authors have outlined the diagnostic problems in patients with TCA 2,4, Atypical symptoms may lead to excessively delayed diagnosis. Patients present with either ileus or symptoms as in typical Hirschsprung's disease but additionally with recurrent vomiting.

In patients presenting with ileus, diagnosis may be delayed for several weeks because causative factors like volvulus or meconium ileus do not primarily warrant investigations for aganglionosis. Furthermore, TCA may be associated with other anomalies of the gastrointestinal tract. Only a few reports of TCA associated with small bowel atresia and volvulus can be found 3, 7. In cases of midgut volvulus without malrotation, aganglionosis has to be ruled out.

Neonatal appendicitis, a very rare disease, may be the leading symptom of TCA. Therefore, rectal biopsies are mandatory in those cases.

Additional to the diagnostic problems due to atypical and heterogenic symptoms, histochemical examination of rectal biopsies may prove negative or equivocal because increased acetylcholinesterase activity may not be present in TCA 5,10, Furthermore, there is no typical radiographic pattern 13, Plain abdominal radiographs usually suggests low bowel obstruction whereas barium enema usually does not show pathognomonic features.

If no mechanical obstruction is found at laparotomy in neonates presenting with ileus, it is suggested to resect the appendix to rule out TCA. If rectal mucosal biopsies are negative or equivocal, biopsies should be repeated or a formal sphincterectomy for thorough analysis is done.

The second period lasts from the raising of stoma to its closure, including the definite surgical procedure. Failure to thrive and excessive fluid losses have been reported in patients with ileostomies 2. Post-ileostomy complications, however, have been eliminated after the importance of oral sodium supplementation to maintain the enteral co-transport system has been realized Interestingly, right transversostomies may show a good function even in cases of TCA.

Therefore, frozen section biopsies are mandatory when raising a stoma. The definitive surgical procedure has been debated 2,5,8,9, Colonic patch graft procedures were the first proposals for surgical management of TCA The rational behind were to use the distinctive resorptive function of part of the aganglionic colon 6.

Use of the right colon has the theoretical advantage of improved water resorption. However the colon patch procedures have significant complications, e. Actually, a modified Duhamel's pull-through procedure seems favorable in the treatment of TCA 2, The third critical phase begins with closure of the stoma.

Complications in this period are predominantly recurrent episodes of sub-ileus and diarrhea or nocturnal incontinence.

The cause for sub-ileus is a raised tone in the residual sphincter. Repeated manual anal dilatations may be mandatory. Side effects of large doses of Loperamide are mental irritability and dyskinesia.

Significantly better survival of the patients with TCA nowadays is mainly attributed to more accurate diagnosis and improved management of infants with ileostomies.

A new approach to total aganglionosis of the colon. Surg Gynecol Obstet Cass DT, Myers N: Pediatr Surg Int 2: Total colonic aganglionosis with or without ileal involvement: A review of 27 cases. J Pediatr Surg Festen C, Severijner R, v. The absorptive function of colonic aganglionoic intestine: Are the Duhamel and Martin procedures rational?

Ikeada K, Goto S: Total colonic aganglionosis with or without small bowel involvement: An analysis of patients. A new surgical approach to extensive aganglionosis. Further experience with the colonic patch graft procedure and long-term results. Suction biopsy in Hirschsprung's disease.

Arch Dis Child A possible cause of anastomotic failure following repair of intestinal atresia. Can J Surg Surgical management of Hirschsprung's disease involving the small intestine.

Improvements in the management of total colonic aganglionosis. Pediatr Surg Int 5: The importance of oral sodium replacement in ileostomy patients. Progr Pediatr Surg Diagnosis of congenital megacolon: J Pediatr Surg 7: Imperforate anus IA is a congenital anomaly in which the natural anal opening is absent.

Diagnosis of IA is usually made shortly after birth on routine physical examination. The incidence of IA is approximately 1 in live births and it is more common in males. Its etiology is unknown and it runs equally through all racial, cultural and socio-economic groups. IA is classified as either "high" or "low" depending on the termination of the distal rectum.

When the rectum ends above the levator muscles the malformations are classified as high, and when the rectum ends below the levator muscles the malformations are classified as low. High lesions are more frequent in males, low ones in females. Determination of the level of the lesion by abdominal x-ray or perineal ultrasound is critical for appropriate management.

Children who have IA may also have other congenital anomalies. Vertebral defects, Anal atresia, Cardiac anomalies, Tracheoesophageal fistula, Esophageal atresia, Renal anomalies, and Limb anomalies.

Repair of low IA is relatively simple and is usually treated with perineal anoplasty; however, repair of high IA is more complex. Patients are initially given a temporary colostomy and time is given to allow the child to grow. A pull-through operation is completed at a later date. Independent of the level of the lesion, the goal of the surgery is the creation of adequate nerve and muscle structures around the rectum and anus to provide the child with the capacity for bowel control.

Male patients will benefit from perineal inspection to check for the presence of a fistula wait hours of life before deciding. During this time start antibiotherapy, decompress the GI tract, do a urinalysis to check for meconium cells, and an ultrasound of abdomen to identify urological associated anomalies.

Perineal signs in low malformations that will NOT need a colostomy are: These infants can be managed with a perineal anoplasty during the neonatal period with an excellent prognosis. Meconium in urine shows the pt has a fistula between the rectum and the urinary tract. Flat "bottom" or perineum lack of intergluteal fold , and absence of anal dimple indicates poor muscles and a rather high malformation needing a colostomy.

Patients with no clinical signs at 24 hours of birth will need a invertogram or cross-table lateral film in prone position to decide rectal pouch position. Those cases with high defect are initially managed with a totally diverting colostomy. Diverting the fecal stream reduces the chances of genito-urinary tract contamination and future damage. These infants require a colostomy before final corrective surgery.

The colostomy can be done electively before discharge from the nursery while the GI tract is decompressed by dilatation of the fistulous tract. A single orifice is diagnostic of a persistent cloacal defect usually accompany with a small-looking genitalia. Cloacas are associated to distended vaginas hydrocolpos and urologic malformations.

This makes a sonogram of abdomen very important in the initial management of these babies for screening of obstructive uropathy hydronephrosis and hydroureter. Hydrocolpos can cause compressive obstruction of the bladder trigone and interfere with ureteral drainage.

Failure to gain weight and frequents episodes of urinary tract infections shows a poorly drained urologic system. A colostomy in cloacas is indicated. Radiological evaluation will be of help along with a diverting colostomy in this cases. Perineal fistulas can be managed with cutback without colostomy during the neonatal period. The most important prognostic characteristic is the severity of the IA. Patients with low IA have a good probability of having normal stool patterns.

Patients with high IA report more problems such as fecal incontinence and constipation. For patients who cannot maintain normal bowel function, the use of a special diet, underpants liners, enemas and drugs have ameliorated their lives. Long-term follow up with both qualitative and quantitative quality of life considerations of these patients is very important. References 1- Chen CJ: The treatment of imperforate anus: J Pediatr Surg 34 Inheritance of familial congenital isolated anorectal malformations: Am J Med Genetics Do children with repaired low anorectal malformations have normal bowel function?

J Pediatr Surg 32 6: Semin Pediatr Surg 4 1: Management of anorectal malformations during the newborn period. World J Surg 17 3: Posterior sagittal approach for the correction of anorectal malformations. Surgical treatment of high imperforate anus. World J Surg 9 2: J Pediatr Surg 17 5: Although intussusception can occur at any age, the greatest incidence occurs in infants between months of age. Over half of the cases are in the first year of life. Frequently occurs after a recent upper respiratory infection, by Adenovirus type 3 that causes a reactive lymphoid hyperplasia that act as lead point of Peyer's patch.

Meckel's diverticulum, polyps, Henoch's Schonlein purpura, hematoma, lymphoma, foreign bodies, and duplications. Most children have no lead point and it is felt that enlarged mesenteric nodes or swollen Peyer's patches may be the cause. The baby has intermittent periods of severe discomfort with screaming, stiffening and drawing up of the legs, followed by periods of rest.

Vomiting may occur and bloody, mucoid currant jelly stool may be passed. The baby may become dehydrated and appear acutely ill. Frequently, lethargy may be an early sign. To be successful, the barium must reflux into the terminal ileum. The surgeon should be notified before an attempt at barium reduction, and should be present at the time of study.

Recently the use of gas enema reduction has been successful in patients with: Ultrasonography can be used as a rapid sensitive screening procedure in the initial diagnosis of intussusception. Previous adverse clinical features that precluded barium reduction can be replaced during gas reduction. Predictors of failure of reduction are: Air reduction pneumocolon is a very effective alternative method since it brings less radiation shorter flouroscopy time , less costs and less morbidity in cases of perforations.

Failure of hydrostatic reduction requires urgent operation through a right lower quadrant horizontal incision. The intussusception is reduced by pushing on the distal bowel like a tube of toothpaste rather than pulling the proximal bowel. Most cases are ileo-colic intussusception, and a few are jejuno-jejunal or ileo-ileal intussusception. The traditional method of diagnosing and managing ileo-colic intussusception is barium enema contrast reduction. In China where this is the most common surgical emergency in childhood, pneumatic reduction has been used for more than 25 years.

A recent tendency toward this approach is seen in recent years in Occident. Small bowel aeration is a sign of complete reduction. Gas enema reduction is very successful in patients with: The condition can occur in an isolated form either localized to colon or disseminated throughout the bowel , or associated to other diseases such as Hirschsprung's HD , neurofibromatosis, MEN type IIB, and anorectal malformations.

Clinically two different types of isolated IND have been described: Type A shows symptoms of abdominal distension, enterocolitis, bloody stools, intestinal spasticity in imaging studies Ba Enema since birth, is less common and associated with hypoplasia of sympathetic nerves. Type B is more frequent, symptoms are indistinguishable from that of HD, with chronic constipation, megacolon, and repeated episodes of bowel obstruction.

Management depends on clinical situation; conservative for minor symptoms until neuronal maturation occurs around the 4th year of life, colostomy and resectional therapy for life threatening situations.

The most common congenital diaphragmatic hernia CDH is that which occurs through the postero-lateral defect of Bochdalek. It is caused by failure of the pleuroperitoneal membrane to develop adequately and close before the intestines returning to the abdomen at the tenth week of gestation. The intestines then enter the pleural cavity and cause poor lung development leading to pulmonary hypoplasia a reduced number of alveoli per area of lung tissue.

This defect is postero-lateral in the diaphragm and may vary in size. Stomach, liver or spleen may be partly in chest as well. The clinical presentation is that the newborn becomes rapidly cyanotic, acidotic, and has poor ventilation. Major findings relate to the degree of pulmonary maldevelopment. Chest films will show intestines in the chest. Placement of a radiopaque nasogastric tube may show the tube coiled in the lower left chest. Higher risk factors are: Treatment consist of rapid intubation and ventilation with use of muscle relaxants, placement of a nasogastric tube to prevent gaseous distension of the intestines and preoperative stabilization of arterial blood gases and acid-base status.

Surgery can be undertaken when one of the following objectives are met: Operative management consist of abdominal approach, closure of hernia by primary repair or use of mesh, and correction of malrotation. Postoperative management is very difficult. Due to hypoplastic lungs, there is frequently pulmonary hypertension leading to right-to-left shunting and progressive hypoxemia, hypercarbia, and acidosis that worsens the pulmonary hypertension.

Sufficient, High Quality Protein. As discussed previously, during the breakdown of dietary protein in the digestive process, waste substances are created which are filtered out of the blood by the kidneys and excrete d via urination. Unfortunately damaged kidneys find it harder to do this, which is why your CKD cat may feel poorly.

You will note the reference to not feeding more protein than your cat's body needs to maintain normal function. This is the crux of the matter. You do not want to feed an extremely low level of protein so your cat suffers weight loss and malnutrition; but nor do you want to be loading your cat's body with unnecessarily high levels of protein which contribute to your cat feeling ill.

The goal in CKD is not to feed low protein or high protein. The goal is to feed sufficient protein with the correct balance and number of amino acids to maintain the cat's health and body weight, but in a form which needs as little breaking down as possible. When talking about CKD, that is what we mean by "high quality protein", not reaching for organic, high quality meat.

In addition to the amount of protein, patients with CKD should receive protein of high biologic value. For most people, the easiest way to achieve this is to feed a therapeutic kidney diet because these diets have a protein level in this range.

This does not mean they are low protein foods. If you find your cat starts to exhibit weight or muscle loss, you could consider trying one of the therapeutic kidney diets with protein at the higher end of the suggested range. A good choice would be egg whites. If you cannot persuade your cat to eat a therapeutic kidney diet see Which Foods to Feed for tips on how to do this , you can also check the food data tables to find other foods which are relatively low in protein; but don't forget the therapeutic kidney diets have other important attributes, and the protein they do contain is good quality from the CKD perspective, something which is not always easy to replicate with non-therapeutic kidney foods.

When To Feed Reduced Protein. IRIS Stages 1 and 2. Because of the potential downsides of protein restriction, it is not necessarily a good idea to feed reduced protein food in all cases. However for cats with proteinuria , it states "feed a renal clinical diet" regardless of the stage the cat is in.

The study concludes "Our results suggest that cats with early renal insufficiency fed a test food designed to promote healthy aging, over a 6 month period, were more likely to have stable renal function evidenced by stable serum SDMA concentrations compared with cats fed owner's-choice foods.

It is also difficult to compare the effect of the therapeutic kidney diet because not enough is known about the alternative foods that were fed. Other vets believe that it is better to wait until the disease is more advanced before starting a therapeutic kidney diet.

M anaging chronic diseases in cats Veterinary Medicine Little S states "Don't restrict dietary protein for cats experiencing mild to moderate chronic renal insufficiency creatinine 1. These cats require adequate protein and calories to maintain body weight and to avoid muscle wasting and anemia. If your cat also has hyperthyroidism, it can be even more of a concern since hyperthyroid cats are prone to weight loss and muscle wasting.

Diet and nutritional management for hyperthyroid cats Peterson ME the man who discovered hyperthyroidism in cats states that "The major problem that I have with some of the prescription kidney diets is that they restrict protein to the point that some cats — especially those with concurrent hyperthyroidism —will continue to catabolize their own muscle mass despite adequate control of the thyroid condition.

Unfortunately, it can often be easier to switch a cat to a reduced protein diet when the cat is stable with lower numbers. Treatment recommendations for CKD in cats International Renal Interest Society says that introducing a therapeutic diet "may be accomplished more easily early in the course of CKD, before inappetance develops. If you are concerned, consider adding foods with high biologic value but minimal nitrogenous waste to your cat's therapeutic kidney diet.

If you decide not to feed reduced protein to your CKD cat, please do ensure that your cat has a low phosphorus intake and an increased essential fatty acids intake. IRIS Stages 3 and 4. Cats who are in Stages 3 and 4 would therefore also be advised to eat a therapeutic kidney diet. Another factor to consider is your cat's BUN level. Since BUN is influenced by protein intake, it does often help the cat feel better if you restrict protein intake as your cat's BUN levels rise.

In Slowing the progression of chronic renal failure Dr GF Grauer states that "As the renal failure progresses, additional dietary protein reduction will likely be necessary. You may panic if you cannot get your cat to eat a reduced protein food. Take a deep breath. M anaging chronic diseases in cats Veterinary Medicine Little S states "Never try to force an anorexic patient with chronic renal insufficiency to eat a protein-restricted diet.

Instead, concentrate on encouraging anorexic patients to eat. See the Which Foods to Feed page for more tips on getting your cat to eat the therapeutic kidney diet and what to do if you can't succeed. Consider feeding tube intervention e. See the Persuading Your Cat To Eat page for more information on feeding tubes and tips on getting your cat to eat. Whatever you do, monitor your cat's weight and muscle status closely.

Controlling phosphorus levels is extremely important for CKD cats, because high phosphorus levels are very damaging to their health and can make the disease progress more quickly. This is such an important topic that I have an entire page devoted to phosphorus control. Please read it and do everything you can to keep your cat's phosphorus levels low - it can make all the difference to your cat's wellbeing and can also prolong survival.

Just as cats need a diet relatively high in protein, so they also need relatively high levels of fat compared to a human or dog. Older cats may process fat less efficiently than younger cats, which may be a factor in weight loss. Fat does not result in a lot of waste products like protein, so processing it is not a strain on the kidneys; plus cholesterol is not an issue for cats the way it is for humans. Studies indicate that cat foods containing even higher amounts of fat are safe.

In most therapeutic kidney foods, the fat content is increased to compensate for the lower protein levels. Some senior cat foods also have relatively high levels of fat and relatively low levels of protein; as a bonus, they often also have low phosphorus levels.

Therefore, if your cat won't eat a therapeutic kidney diet, it is worth considering senior foods, although do check the protein level is not too low. The kidneys cannot process sodium as effectively in CKD, which increases the risk of hypertension high blood pressure in humans.

It used to be thought that the same applied to cats, and it was therefore recommended that sodium intake should be restricted. Research in Applied Veterinary Medicine 7 4 pp found that sodium intake appeared to have no effect on in blood pressure in CKD cats, but that levels of BUN, creatinine and phosphorus were higher in the cats eating a high sodium diet compared to those eating a low sodium diet.

Even in cats with creatinine over 1. These results are consistent with the majority of other studies evaluating sodium intake in cats, as well as with the National Research Council's assessment, all of which indicate that sodium at 1. Effects of dietary salt intake on renal function: The study concludes "The results of this 2 year study do not support the suggestion that chronic increases in dietary salt intake are harmful to renal function in older cats.

Increased dietary sodium increases urine output and may decrease the risk of forming calcium oxalate uroliths due to the decrease in relative supersaturation of solutes. However, caution should be used in increasing the sodium intake of patients with renal disease as increased dietary sodium may have a negative effect on the kidneys independent of any effect on blood pressure. So should you restrict sodium intake or not? Treatment recommendations for CKD in cats International Renal Interest Society states on page 5 that there is no evidence that reducing sodium intake is helpful for CKD cats, and that it should certainly not take the place of medication for hypertension , but if you do opt to reduce your cat's sodium intake, you should do it gradually.

The food data tables provide information about the sodium content of many cat foods available in the USA and UK. This occurs because potassium is easily lost through increased urination and vomiting. Therapeutic kidney diets contain extra potassium all cat foods need some potassium , and this is usually in the form of potassium citrate, because potassium citrate may help with a problem seen in some CKD cats called metabolic acidosis.

If your cat refuses to eat a therapeutic diet, your vet can give you a potassium supplement instead, if appropriate; some cats need a potassium supplement whether or not they eat the therapeutic kidney diet. Many commercial cat foods are acidified in order to reduce the risk of FLUTD feline lower urinary tract disease.

These foods often say that they are designed to maintain urinary tract health; or they may contain cranberries or additional Vitamin C. However, these foods which are actually designed to treat a different kind of problem to CKD may have the effect of increasing the amounts of potassium lost in the urine, which is bad for CKD cats.

It is therefore best not to feed acidified foods to CKD cats, who tend to have quite high acid levels anyway. Please see the Potassium page for more information about potassium. It also states "Our analysis indicates that cats have a ceiling for carbohydrate intake, which limits ingestion and constrains them to deficits in protein and fat intake relative to their target on high-carbohydrate foods.

In The carnivore connection to nutrition in cats Zoran D Journal of the American Veterinary Medical Association pp, Dr Zoran writes "It is clear that cats have a greater need than dogs or other omnivores for protein in their diet. Cats also have several physiologic adaptations that reflect their expected low CHO [carbohydrate] intake These specific differences do not mean cats cannot use starch. In fact, cats are extremely efficient in their use of simple sugars.

However, it does underscore their development as carnivores and the expected low amounts of grain in their typical diet. These digestive differences may mean that high amounts of CHO in diets may have untoward effects on cats. Therefore, if you are trying to reduce your CKD cat's protein intake, I would recommend increasing the fat in the diet see above rather than the carbohydrates.

If you are feeding a therapeutic kidney diet, this will often be done automatically - many of these diets increase the fat content rather than the carbohydrates in order to offset the reduced protein content.

Pet Education has an interesting article about carbohydrates in the feline diet. Fibre is the non-digestible component of complex carbohydrate. It is important for good digestive health. Increased fibre may help with elevated calcium levels in the body hypercalcaemia , although one type of fibre, fructooligosaccharides or FOS, may actually increase calcium levels in the body see below.

It may also assist with two commonly seen CKD problems, toxin reduction and the control of constipation. There are a number of ways of categorising fibre types, but one way is to divide it into fermentable and non-fermentable. Which fibres are fermentable depends upon the species of bacteria eating the fibre in the cat's gastrointestinal tract. Diet and large intestinal disease in dogs and cats JW Simpson The Journal of Nutrition SS has a table showing soluble and fermentable fibres.

In terms of general health, you do not necessarily want the most fermentable fibres. Dietary fiber for cats: It concludes that the diet "which contained the most fermentable fibers, severely decreased nutrient digestibility and resulted in poor stool characteristics.

Diets that contain moderately fermentable fiber provide fermentation end products that may be important in maintaining the health of the gastrointestinal tract of the cat. There has long been interest in whether other bodily mechanisms might be useful for relieving the load on damaged CKD kidneys.

Bowel as a substitute in renal failure EA Friedman American Journal of Kidney Diseases 28 6 pp states "Extraction, modification, or recycling of nitrogenous wastes by the gastrointestinal tract is a potentially low-cost means of substituting for missing renal function. Multiple approaches to the bowel as a substitute kidney have been attempted.

One way of doing this may be via increased fibre intake in the form of fermentable fibre prebiotics. Fermentable fibre provides a source of carbohydrate for the bacteria in the gut. These bacteria, which are essential to health, increase in number when provided with additional fermentable fibre, and the more bacteria there are, the more nitrogen is excreted in the faeces. This increased faecal excretion may help to reduce the load on the kidneys by diverting the excretion of urea from the kidneys.

You can read more about this in the Treatments chapter. Non-fermentable fibre can be helpful for CKD cats because it reduces the risk of constipation, a common problem in CKD cats, by holding water in the stool. Most commercial cat foods have sufficient levels of fibre for a healthy cat, but if your cat suffers from constipation you may wish to add more fibre in the form of something such as pumpkin, baby peas or psyllium. Please see Constipation for more information on dealing with constipation.

Feline Constipation explains more about fibre and gut health. Side Effects and Interactions. Some forms of fibre, such as fructooligosaccharides FOS , may also bind calcium in the small intestine and lead to an increase in calcium levels in the body hypercalcaemia. This can be a problem for cats who already have high blood calcium levels. Inulin and guar gum may do this, as may slippery elm bark and lactulose , two treatments commonly used for constipation in CKD cats.

Fibre may also affect taurine levels in some foods. I would therefore recommend discussing additional fibre with your vet before adding it, and avoiding its use in a cat who already has high calcium levels. They are essential because the cat's body cannot synthesise them in sufficient amounts, so they have to be obtained from food.

Commercial diets tend to contain far more Omega-6, partly because Omega-6 EFAs are cheaper and more stable, but this may create a potentially harmful imbalance. The correct balance is not yet known, though some believe it is probably around 5: Essential fatty acids are important for many bodily functions. It has been known for many years that they have an effect on the skin - the first signs of an imbalance or deficiency are usually a dry coat, itchy skin or matted fur. Recently it appears that they may have an important role in controlling inflammation.

Research in rats and humans indicates that the addition of omega-3 fatty acids to the diet may delay the progression of CKD. Small Animal Practice 38 1 pp added essential fatty acid supplements in the form of fish oil to dog foods. It concludes "newer data indicate that dietary supplementation with specific antioxidants is an important consideration for limiting renal oxidant stress and progression of CKD. Nutritional management of renal disease: Dietary omega-3 fatty acid supplementation in the form of fish oil can have beneficial effects in reducing GCP.

This ties in with what one kidney specialist vet has informed me, that oversupplementation can throw off the correct ratio of Omega-3s to Omega-6s, and might be detrimental in some cases. Omega-3 fatty acid supplementation for dogs and cats with heart disease Nutrition Service at Cummings Veterinary Medical Center at Tufts University states "Potential risk factors include decreased platelet function and coagulation, and possibly suppressed wound healing Other potential effects include soft feces, diarrhea, flatulence, vomiting, and halitosis.

Nutrition and renal function: At higher levels of supplementation, renal function was actually increased in normal cats. These data support the assertion that this dietary maneuver is safe for normal cats and provides some encouragement for further consideration for dietary n-3 PUFA supplementation in cats with renal disease, systemic hypertension, or hypersensitivity reactions.

Almost everybody I know of who has added essential fatty acids to their cat's treatment plan, whether in a therapeutic kidney diet or as a supplement, has been happy with the results, reporting an improvement in general wellbeing. Additional EFAs do cause vomiting in some cats though, and I've heard from a number of people whose cats had pancreatitis and who felt essential fatty acids did not agree with these cats, causing problems such as diarrhoea.

However, there are no reports of omega-3 fatty acid or fish oil supplements causing pancreatitis in dogs, cats, or humans. Theoretically, omega-3 fatty acids could prevent pancreatitis because of decreased blood triglyceride concentrations.

An extremely high dosage of omega-3 fatty acids or a fish oil supplement in addition to a very high fat diet would likely be required to induce pancreatitis. An increased level of essential fatty acids compared to standard cat foods is one of the features of therapeutic kidney diets. If you wish to give additional essential fatty acids, ask your vet if they are appropriate for your cat. Since cats as obligate carnivores benefit from animal-based products, the most appropriate form of essential fatty acid supplement is fish oil.

Oils from the liver, such as cod liver oil, are not suitable because they contain too much Vitamin A and D. Omega-3 fatty acid supplementation for dogs and cats with heart disease Nutrition Service at Cummings Veterinary Medical Center at Tufts University states "We also recommend avoiding cod liver oil for this purpose as it is too high in vitamins A and D when administered at this dose and can cause toxicity of these vitamins.

If fish oils are given, extra vitamin E is also required in order to avoid a problem called steatitis. Waltham International Symposium ppSS discusses this. Many products, especially veterinary ones, already contain vitamin E in an appropriate dosage it may be referred to as tocopherol , in which case you do not need to supplement Vitamin E. However, I would ask your vet how much to give, because too much vitamin E can be dangerous. It has been on the market since January The manufacturer states that the product was tested on an informal basis on 18 CKD cats in the Montreal area over a period of about eight months.

This product is basically a combination of essential fatty acids, Vitamin E which you need to add when you are supplementing fish oils, but which is also an antioxidant and CoQ10 ubiquinol , also an antioxidant, but in a concentrated formula. You can read more about it in the Treatments chapter. Some people prefer to give krill oil to their cats because they find their cats tolerate it better. Krill oil is made from crustaceans rather than fish and contains additional antioxidants called astaxanthin and canthaxanthin.

The essential fatty acids in krill oil are phospholipids in fish-based oils they are triglycerides. This was due to increased urinary P excretion associated with the phospholipids content of these oils sources. Although further studies are needed, susceptible individuals should be aware of a potential risk of increasing phospholipids consumption on renal health. Personally, I think I would be more comfortable using fish oil.

If you are in Europe, especially Italy, you may be offered a new product called Nefrokrill, which contains potassium citrate , lanthanum carbonate a phosphorus binder and essential fatty acids. You can read more about it here. Vegetable-based oils , such as coconut oil or olive oil or flax seed linseed oil , are not recommended, because they do not contain the essential fatty acids which a cat needs.

Essential Fatty Acids Dosage. It can be a bit tricky working out an appropriate dose of essential fatty acids for cats. The National Research Council gives an upper limit for dogs but gives no upper limit for cats. As far as fish oils are concerned, Pet MD discusses the dangers of giving too much but says that if you take the NRA recommendations for dogs, "Translating the data suggests that a dose between mg combined EPA and DHA per pound of body weight is safe for dogs and cats.

This dose is far less than those used to treat serious conditions where the risk of side effects is less important. Top 5 therapeutic uses of Omega-3 fatty acids Chandler ML Clinician's Brief Feb pp states "the amount to supplement is somewhat empiric and depends on the amount in the diet. The higher dosages often are used to lower serum triglyceride concentrations in patients with hypertriglyceridemia, whereas lower dosages are more commonly used for inflammatory conditions, renal disease, and cardiac disease.

There are a small number of commercial pet foods that contain this dose for example, the Royal Canin Early Cardiac Diet for Dogs. However, in most cases, supplements are needed to achieve this dose. As you can see, there is no definitive dose, and many of the recommendations relate to a particular amount of EPA eicosapentaenoic acid. So if your cat weighs 8 lb 3. You will need to check the product you're considering to see how much EPA it contains.

Many fish oil capsules are mg strength. I expect your head is spinning by now! Generally speaking, it is probably safe to give your cat one mg fish oil capsule daily. The DHA in salmon may also help your mood. Studies suggest it may play a role in preventing postpartum depression. The FDA recommends that breastfeeding women, women who are pregnant, and women who might get pregnant limit how much salmon they eat. The guidelines recommend an average of 12 ounces, or the equivalent of two main servings, per week.

The reason is to limit the amount mercury your new child is exposed to. The mercury level in salmon is considered low. Some other fish, such as swordfish or mackerel, have a high amount of mercury and should be avoided altogether. The 12 ounces are an average. Eating more in 1 week -- such as having three servings instead of two -- won't hurt as long as you eat less the following week.

Whether you prefer yogurt, milk, or cheese, dairy products are an important part of healthy breastfeeding. Milk delivers a boost of bone-strengthening vitamin D. In addition to providing protein and B vitamins , dairy products are one of the best sources of calcium. If you're breastfeeding , your milk is loaded with calcium to help your baby's bones develop, so it's important for you to eat enough calcium to meet your own needs.

Try including at least three cups of dairy each day in your diet. Boost your energy as a new mom with iron-rich foods like lean beef.

A lack of iron can drain your energy levels, making it hard for you to keep up with the demands of a newborn baby.

Nursing moms need to eat extra protein and vitamin B Lean beef is an excellent source for both. Iron-rich beans, particularly dark-colored ones like black beans and kidney beans, are a great breastfeeding food, especially for vegetarians.

Breastfeeding moms should be sure to get two or more servings of fruit or juice each day. Blueberries are an excellent choice to help you meet your needs. These satisfying and yummy berries are filled with good-for-you vitamins and minerals, and they give you a healthy dose of carbohydrates to keep your energy levels high.

You might be tempted to cut back on carbs to help lose the baby weight. Losing weight too quickly may cause you to make less milk and leave you feeling sluggish.

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