When a baby is born, parents want nothing more than to love and protect their child. Part of that protection starts right after birth with the administration of a vitamin K injection. Babies are not born with sufficient vitamin K levels and cannot get adequate amounts of vitamin K from breast milk, so this injection, given within the first hour after birth, is crucial because it helps a baby’s blood to clot normally, which prevents vitamin K deficiency bleeding (VKDB) in newborns. A recent CDC report confirmed that there has been a nationwide increase in parents refusing the vitamin K shot for their newborns— and this dangerous trend, often based on inaccurate information found online and faulty science, is causing more babies to experience hemorrhaging that is preventable and may cause brain damage or even death in some cases. In the United States, administration of intramuscular vitamin K at birth to prevent all forms of VKDB has been standard practice since first recommended by the American Academy of Pediatrics in 1961.
Without the shot, the incidence of early and classical VKDB ranges from 0.25% to 1.7% of births and the incidence of late VKDB ranges from 4.4 to 7.2 per 100,000 infants. The relative risk for developing late VKDB has been estimated at 81 times greater among infants who do not receive intramuscular vitamin K than in infants who do receive it. Early VKBD usually presents in previously healthy appearing infants as unexpected bleeding during the first two weeks of age, usually between the second and fifth day after birth. The bleeding can present as oozing from the umbilical cord area, bleeding from the circumcision site, persistent oozing from puncture sites, gastrointestinal hemorrhage, and/or bleeding into the brain, which can result in significant neurological complications that have a lifelong impact on a child. Late VKDB is an indication of severe vitamin K deficiency and presents as unexpected bleeding, including brain bleeds in infants 2-12 weeks of age. Complications of late VKDB may be severe, including death.
It classically presents in exclusively breastfed infants who received either no or inadequate neonatal vitamin K. It can also present in infants with intestinal malabosorption defects. One myth about vitamin-k injections is that they are linked to leukemia, but studies show absolutely no relationship between getting vitamin K as a baby and an increased risk of leukemia. Another myth is that the vitamin K injection increases the risk of jaundice—which is inaccurate. Jaundice associated with vitamin K has been observed only in high risk babies (such as premature babies) in doses 30-60 times higher than the dose we give. Some parents also argue that injections cause babies pain, but this pain is very brief and the benefits of the injection are very much worth a short period of discomfort. Parents are encouraged to mitigate this brief uncomfortable experience by holding baby skin to skin before and after the injection or allowing the baby to breastfeed before, during and/or after getting the injection.
In the not so distant past, infants and children had high rates of dying early in life. During the 20th century alone, the infant mortality rate declined greater than 90% and the maternal mortality rate declined 99%! Much of this is due to advancements in modern medicine. While it might seem nice to do things completely naturally, modern medicine has saved the lives of countless mothers and babies. Update: For more information on this subject, Dr. Lauren Marcewicz, a pediatrician with CDC’s Division of Blood Disorders, speaks about vitamin K deficiency bleeding in infants, the importance of vitamin K prophylaxis at birth, and how healthcare providers can provide the best information to their expectant parents. Listen to the podcast by clicking here now.Volume 52, Issue 1, March 2014, Pages 22–29 The causes of obstructive jaundice are varied, but it is most commonly due to choledocholithiasis; benign strictures of the biliary tract; Surgery in patients with obstructive jaundice is generally considered to be associated with a higher incidence of complications and mortality.
Therefore, it poses a considerable challenge to the anesthesiologist, surgeons, and the intensive care team. However, appropriate preoperative evaluation and optimization can greatly contribute to a favorable outcome for perioperative jaundiced patients. This article outlines the association between obstructive jaundice and perioperative management, and reviews the clinical and experimental studies that have contributed to our knowledge of the underlying pathophysiologic mechanisms. Pathophysiology caused by obstructive jaundice involving coagulopathies, infection, renal dysfunction, and other adverse events should be fully assessed and reversed preoperatively. The depressed cardiovascular effects of obstructive jaundice are worth noticing because it has complicated mechanisms and needs to be further explored. Alterations of anesthesia-related drugs induced by obstructive jaundice are varied and clinicians should be aware of the possible need for a decrease in the anesthetic dose. Recommendations concerning the perioperative management of the patients with obstructive jaundice including preoperative biliary drainage, anti-infection, nutrition support, coagulation reversal, cardiovascular evaluation, perioperative fluid therapy, and hemodynamic optimization should be taken.
Patency of the biliary tree and free drainage of bile into the intestine are important for normal hepatic function. Substances normally excreted into the bile will accumulate in the vascular system owing to obstruction of the biliary tree and the inability to excrete bile into the intestine. These substances, including bile salts, have systemic toxic effects.1 Patients with obstructive jaundice are inclined to develop nutritional deficits, infectious complications, acute renal failure, and impairment of cardiovascular function. Adverse events such as coagulopathy, hypovolemia, and endotoxemia can be insidious and significantly increase mortality and morbidity. Postoperative morbidity of patients with obstructive jaundice is up to about 20–30%.2 The anesthesiologist and critical care team play a crucial role in the perioperative management of such patients.Choledocholithiasis undoubtedly is the leading cause of biliary obstruction, although malignancies such as cholangiocarcinoma, periampullary and pancreatic cancers, and benign stricture including chronic pancreatitis have become increasingly prevalent.3, 4 and 5 It is not surprising that iatrogenic injury of biliary tract and cholangitis are becoming more important with the increase of invasive procedures performed on the biliary tract.
In China, but much less frequently in the USA, parasites absorb nutrition by attaching themselves to the walls of the bile duct, causing bile duct obstruction and fibrosis.6 and 7Long-term obstruction of bile can induce pathophysiological changes involving malnutrition, acute renal failure, and infections that may be fatal. Prolonged obstruction of bile can lead to: malabsorption of fats and steatorrhea; poorly absorbed fat-soluble vitamins because of impaired enterohepatic circulation; susceptibility to night blindness because of vitamin A deficiency; vitamin D deficiency and chronic cholestasis contributing to hepaticosteopathy; and neuromuscular weakness in children attributable to vitamin E deficiency.8 Deficiency of vitamin K requires vigilance especially when invasive procedures are implemented, because vitamin K plays an important role in blood coagulation. Prolonged prothrombin time is attributed to lack of vitamin K-dependent clotting factors resulting from vitamin K deficiency.
If vitamin K deficiency is not treated, patients will bleed easily, resulting in unnecessary blood loss during the perioperative period.9 Sepsis may also deteriorate disseminated intravascular coagulation. In these conditions, necessary precautions should be implemented.The presence of liver disease or a prolonged partial thromboplastin time or active hemorrhage usually indicates a serious prognosis, but appropriate replacement therapy is indicated in this situation.10 Reversal of coagulopathy is the premise not only in case of intraoperative bleeding but also for the insertion of an epidural catheter preoperatively. Hepatocellular dysfunction results in insufficient protein synthesis, gluconeogenesis, and ketogenesis disorders. Therefore, malnutrition is stubborn to correct if obstructive jaundice is not relieved promptly.11 When coagulopathy is present, it can be corrected with intramuscular vitamin K (1–10 mg). When liver failure is present, synthetic function should be the main priority for improvement.
Fresh frozen plasma should be administered intravenously in emergency situations.12 Patients with obstructive jaundice need to replenish nutrients preferably through the enteral pathway. If enteral nutrition is not allowed because of gastric dilatation, clinicians should consider a nasojejunal tube feeding. If enteral nutrition is not available and meanwhile severe malnutrition exists, defined as recent weight loss of >10–15% or actual body weight <90% of ideal body weight, parenteral nutrition can be adopted 5–7 days prior to the operation and continued after the operation.The tendency of bacteria accumulated in bile to develop into infectious complications is also an important consequence of obstructive jaundice. The sphincter of Oddi presents a barrier to retrograde bacteria of the intestine under normal physiological conditions. It is believed that bacteria routinely regress into the biliary tract from the intestine.13 However, bile salts can limit their proliferation,14 and they are efficiently eliminated from bile by the reticuloendothelial system.
Furthermore, bile excretion from the bile tract into the intestine can also clear bacteria.3, 13, 14, 15, 16 and 17 Flemma et al13 reported that bacteria were more easily cultured from bile of patients with partial biliary obstruction than with complete biliary obstruction. This indicates that retrograde contamination of bile may be an essential factor. Alternatively, bacteria may contaminate bile possibly through the hepatic artery, the portal venous systems, or even biliary lymphatics.14 and 16 Furthermore, with the absence of biliary intervention, sepsis may occur because of a combination of gut failure with increased bacterial translocation through the portal system or significant biliary colonization.18 and 19 The incidence of bacterial contamination increases in patients with sphincterotomy or cholangioenterostomy and in those treated with internal biliary drains and biliary stents. About two-thirds of patients with malignant obstructive jaundice have positive bacterial cultures of bile after initial endoscopic retrograde cholangiopancreatography.
Patients with a biliary intervention have a colonized rate of almost 100%, and these infections tend to be polymicrobial. Repeated reflux of bacteria and endotoxin into the vascular system eventually leads to systemic inflammatory response syndrome and even sepsis.Bacteria isolated from bile of patients with cholangitis mainly include Gram-negative organisms: usually Escherichia coli and Klebsiella, Proteus, Pseudomonas species; and Gram-positive organisms: mainly Streptococcus and Enterobacter species. 15, 20, 21, 22, 23, 24 and 25 A β-lactam inhibitor combined with aminoglycoside can be used empirically. Quinolones and carbapenams excreted into the bile are generally effective monotherapy in the treatment of cholangitis. 26, 27 and 28 Enterococci and anaerobes targeted antibiotics can also be used in those who have antibiotic resistance, and in those with previous biliary intervention and elderly patients. 29 and 30 However, antibiotics alone are unlikely to be effective until effective biliary drainage has been done.