case study on jaundice slideshare

DNB Pediatrics

Pediatric history taking | infant with jaundice.

Introduction / Opening the consultation

XYZ, an 8 months old girl baby, 1st born to non-consanguineously married parents, xxx by religion, resident of xxx, presented to the outpatient department accompanied by mother for her follow-up today. Informant is mother xxx, who seems a reliable source for history.

Chief complaints

• Yellowish discoloration of skin and urine since 2 months of age
• Pale colored stool since 2 months of age

History of presenting illness

Here the history dates back to 2 months of age and the clinical condition seems to be antenatal in origin. In such cases, it is reasonable to start from antenatal or natal history in HOPI. You can mention that while presenting the case.

Antenatal history

This was the first pregnancy of a 25-year-old mother, Lata. She was registered case and received iron, folic acid, calcium, and antenatal immunization. She has had no history of complications like diabetes, hypothyroidism, or hypertension during ANC. No H/O fever, rash, lymphadenopathy. The ultrasound scans were done, both normal.

Natal history

XYZ (use name often than 'patient') was delivered by a normal vaginal route at term vigorously and required only routine newborn care after delivery. The birth weight was 2.4 kg. There was no history of PROM or difficult/instrumental delivery.

Postnatal history

As a baby xyz was started on breastfeeding within an hour after birth and passed meconium and urine on day 1. She was discharged the very next day. She was been provided usual neonatal care and the mother reports no concerns until 6 weeks of age. She continued to receive usual immunization but no concerns were reported wither by the health care worker/vaccinator confirming her history.

Around 2 months of age, mother noticed dark yellow staining of diaper though stool was pale colored. Upon consulting a local doctor and some tests were done. Mum was informed about a liver problem and she was referred to another center for further investigation and management. They were further advised for a surgical procedure but it was refused. They opted for alternative medicines. We do not have details of those medications or therapy.

At 6 months of age, XYZ got admitted with episodes of vomiting blood along with bluish swellings/spots on the skin. She was then treated with IV antibiotics, blood transfusion, and other IV medications. We do not have a record of these at present. She remained hospitalized for 12 days and was then discharged with oral medications, again no records are available or according to the record/summary the medications were......

Since her last admission, xyz is under regular follow-up. She is on regular oral medications (mention names). Her stool is still pale colored and her urine is dark-colored.

She is relatively well and keeping with her peer's in development. Parents have been counseled that her condition is irreversible and are slowly adapting to the difficult situation.

Negative history/history on leading questions

History to ascertain etiology.

• Maternal history of drug ingestion,
• Jaundice/ infection in pregnancy, for viral illness CMV, Rubella, Hep B.
• Neonatal umbilical catheterization
• Progressive abdominal distension - Storage disorder
• Cardiac disease symptoms for chronic congestive liver failure
• Dysmorphic features - Congenital syndromes
• Family history of hemolytic anemia

History of complications

• Bleeding from any site eg hematurea - coaguloapthy
• Altered sensorium - encephaopathy
• Abdominal distention - Ascites
• Hisotry of pruritis - Cholestasis
• Fever - Secondary infections
• Respiratory distress - secondary to large ascites, secondary resp infection
• Paleness - for anemia

Developmental history

Gross motor.

• Head Control @ 6m
• Rolling over now
• Grasp object
• Transfers from hand to hand.
• Prefers mother
• Appreciate mirror image.

Conclude your findings. Gross motor delay is present. Developmental age is ----.

Immunization history

Give a detailed account of immunization if asked. Keep it ready by enquiring during history taking, Go through immunization record if available.

Nutrition history

XYZ was Exclusively breastfed till 6 months. Then rice-based complementary feeding was started. She is not taking her feed well since her last hospital admission and has not gained appropriate weight since then.

Detail account of food content can be asked. Be ready with calorie requirements for the age and calorie as well as protein gap.

Family history

• Draw 3 generation pedigree.
• Mention if there is any significant family history that can give clues toward the current illness.

Socio-economic history

Socio-economic status of the family, Monthly expenses for the child, attitude of caregiver, whether they are getting any help from Govt or NGOs.

Treatment history

Summarised details of drugs, side effects, progress of symptoms, invasive procedures etc.

Sign-posting/ summarizing history

8 month old girl with pale stool and dark-colored urine, likely to be a case of conjugated hyperbilirubinemia admitted as a part of regular follow-up.

The differentials based on history could be

• Biliary atresia, choledocal cyst, congenital infections, metabolic cause.
• (most likely BA as they were offered surgery at 2 months)

Viva Questions could be

• Storage disorders presenting with Jaundice in Infant
• Bilirubin pathway
• How to differentiate between conjugated vs unconjugated hyperbilirubinemia etc
• Add more in comment box below

Physical Examination

Opening remarks

what is the first impression after you examined xyz. For eg, does she looks well, is she anxious, or sitting comfortably. Are their obvious striking feature like deeply jaundiced malnourished etc.

General Examination

• Vitals - PICCLE
• Antropometry - Height, weight, Chart on percentile graph. Grade of malnutrition if any.
• Head to toe examination.

All dysmorphic features like that of Down’s Syndrome, hypothyroidism or Alagille syndrome.

Signs of vitamin deficiency are important in case of liver cell failure. eg muddy sclera, rachitic features, dry skin, subcutaneous bleeding spots.

Summarise finding

XYZ has stable vitals along with findings of Jaundice, bruises, and Grade 1 malnutrition.

Systemic examination

• Inspection: Localized bulge, distension (which quadrant is more affected)
• Palpation: Superficial palpation: Guarding, tenderness, rigidity
• Tender/Nontender
• Surface: Smooth/Nodular
• Span and Size
• Border: well felt/ sharp/diffuse
• Consistency: Soft/firm/hard
• Size (Grades of splenomegaly)
• Consistency: Soft/firm
• Splenic notch
• Deep Palpation: Kidneys/Divarication of recti/ Hernial sites
• Percussion: Shifting dullness/horseshoe dullness/fluid thrill. Puddle’s sign
• Auscultation: Renal Bruit, Venous hum
• Other systems: Cardiac murmur, hydrocephalus, Meningitis

Here is a detailed proforma of abdominal examination in case of hepatosplenomegaly .

Other systemic examination

• Cardiovascular - Signs of congestive heart failure, hemic murmur due to anemia
• Respiratory - Secondary resp infection, effusion secondary to hypoproteinemia
• CNS - Encephalopathy

Summarise positive findings from the history and physical examination and put your differentials.

A case of conjugated type jaundice with umbilical hernia along with signs of vitamin deficiency, Grade 1 malnutrition, mild - gross motor delay without signs of dysmorphism. There are no signs of portal hypertension or liver cell failure.

The most likely diagnosis could be to be chronic cholestasis of infancy and the most likely etiology could be biliary atresia. Other likely differentials could be neonatal hepatitis, inborn errors of metabolism or chromosomal disorders.

More from Mandira- Infant with cataract

Mandira Roy | DNB(Pediatrics), fellowship in Developmental Pediatrics

Mandira has completed her pediatric residency at the Institute of Child health Kolkata and currently working as a Pediatrician with a special focus on developmental medicine

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Original Author(s): Dr Phil Jordan and Dr Umberto Piaggio Last updated: 16th February 2021 Revisions: 19

• 1 Introduction
• 2.1 Physiological jaundice
• 2.2 Pathological jaundice
• 3 Risk factors and history
• 4 Clinical Presentation
• 5.1 Bilirubin
• 5.2 Further investigations
• 5.3 As needed
• 6.1 Phototherapy
• 6.2 Fluid intake
• 6.3 Exchange Transfusion
• 6.4 IV Immunglobulin
• 7 Complications
• 8 Prognosis
• 9 References

Introduction

Jaundice is t he yellow colouring of skin and sclera caused by the accumulation of bilirubin in the skin and mucous membranes.

Neonatal jaundice  occurs in 60% of term infants and 80% of preterm infants [1] and is caused by hyperbilirubinaemia that is unconjugated (divided into physiological or pathological) or conjugated (always pathological).  High levels of unconjugated bilirubin have acute harmful effects as well as long term damage if left untreated, such as kernicterus .

10% of breast fed babies are jaundiced at 1 month.

Types of Jaundice

Physiological jaundice.

Jaundice in a healthy baby, born at term, is normal and may result from:

• Increased red blood cell breakdown: in utero the fetus has a high concentration of Hb (to maximise oxygen exchange and delivery to the fetus) that breaks down releasing bilirubin as high Hb is no longer needed
• Immature liver not able to process high bilirubin concentrations

Starts at day 2-3, peaks day 5 and usually resolved by day 10.   The baby remains well and does not require any intervention beyond routine neonatal care.

Physiological jaundice can progress to pathological jaundice if the baby is premature or there is increased red cell breakdown e.g. Extensive bruising or cephalohaematoma following instrumental delivery.

Pathological jaundice

Jaundice which requires treatment or further investigation.

• Onset less than 24 hours
• ?previous siblings treated for jaundice/family history/maternal rhesus status
• Maternal blood group (type O most likely to produce enough IgG antibodies to cause haemolysis)
• Requires investigation and treatment
• Onset after 24 hours
• likely dehydrated ?breast fed baby establishing feeding
• increased haemolysis due to bruising/cephalohaematoma
• Unwell neonate: jaundice as a sign of congenital or post-natal infection
• Metabolic: Hypothyroid/pituitarism, galactosaemia
• Breast milk jaundice: well baby, resolves between 1.5-4 months
• GI: biliary atresia, choledhocal cyst

Risk factors and history

Risk factors for pathological hyperbilirubinaemia: to be asked in history

• Prematurity, low birth weight, small for dates
• Previous sibling required phototherapy
• Exclusively breast fed
• Jaundice <24 hours
• Infant of diabetic mother

Clinical Presentation

• Colour: All babies should be checked for jaundice with the naked eye in bright, natural light (if possible). Examine the sclera, gums and blanche the skin. Do not rely on your visual inspection to estimate bilirubin levels, only to determine the presence or absence of jaundice.
• Drowsy: difficult to rouse, not waking for feeds, very short feeds
• Neurologically: altered muscle tone, seizures-needs immediate attention
• Other: signs of infection , poor urine output, abdominal mass/organomegaly, stool remains black/not changing colour

Investigations

• Transcutaneous bilirubinometer (TCB) can be used in >35/40 gestation and >24 hours old for first measurement. TCB can be used for all subsequent measurements, providing the level remains <250 µmol/L and the child has not required treatment
• Serum bilirubin to be measured if <35/40 gestation, <24 hours old or TCB >250 µmol/L
• Infants that are not jaundice to the naked eye do not need routine bilirubin checking.  
• Total and Conjugated Bilirubin is important if suspected; liver or biliary disorder, metabolic disorder, congenital infection or prolonged jaundice. Do not subtract conjugated from total to make management decisions for hyperbilirubinaemia.

Further investigations

• Serum bilirubin for all subsequent levels
• Blood group (Mother and Baby) and DCT
• FBC for haemoglobin and haematocrit
• U&Es if excessive weight loss/dehydrated
• Infection screen if unwell or <24 hours including Microbiological cultures if infection suspected: blood, urine, CSF. Consider TORCH screen.
• Glucose-6-phosphate dehydrogenase especially if Mediterranean or African origin
• LFTs if suspected hepatobiliary disorder

Phototherapy

Figure 1 – NICE treatment threshold graph [3]

• Above: If level is on or above the phototherapy line for their gestation and age (in days) phototherapy should be initiated and bilirubin monitored
• >50µmol/L below, clinically well with no risk factors for neonatal jaundice do not routinely repeat level
• <50µmol/L below, clinically well repeat level within 18 hours (risk factors present) to 24 hours (no risk factors present)
• Repeat bilirubin 4-6 hours post initiation to ensure not still rising, 6-12 hourly once level is stable or reducing.
• NB. Maximum skin coverage, eye protection for babies, breaks for breastfeeding/nappy changes/cuddles to be coordinated to maximise phototherapy
• Stop phototherapy once level >50µmol/L below treatment line on the threshold graphs
• Check for rebound of hyperbilirubinaemia 12-18 hours after stopping phototherapy

Fluid intake

Do not give additional fluids with phototherapy unless indicated and if possible expressed maternal milk is preferred. If phototherapy intensified or feeding poorly consider NGT feeding or IV fluids.

Give consideration to underlying cause i.e. infection, biliary obstruction

Exchange Transfusion

This is the simultaneous exchange of the baby’s blood (hyperbilirubinaemic) with donated blood or plasma (normal levels of bilirubin) to prevent further bilirubin increase and decrease circulating levels of bilirubin.

Performed via umbilical artery or vein and is indicated when there are clinical features and signs of acute bilirubin encephalopathy or the level/rate of rise (>8.5µmol/L/hour) of bilirubin indicates necessity based on threshold graphs. This will require admission to an intensive care bed.

IV Immunglobulin

IVIG can be used as adjunct to intensified phototherapy in rhesus haemolytic disease or ABO haemolytic disease.

Complications

Kernicterus , billirubin-induced brain dysfunction, can result from neonatal jaundice. Bilirubin is neurotoxic and at high levels can accumulate in the CNS gray matter causing irreversible neurological damage . Depending on level of exposure, effects can range from clinically undetectable damage to severe brain damage.

Depends on underlying cause but if correctly and promptly treated prognosis is excellent.

Always refer to local trust guidelines.

1st Author: Dr Phil Jordan

Senior Reviewer: Dr Umberto Piaggio

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• v.9; Jan-Dec 2023
• PMC10722953

Neonatal Jaundice Management: Improving Clinical Knowledge of Jaundice for Improved Attitudes and Practices to Enhance Neonatal Care

Edem kojo dzantor.

1 Department of Epidemiology and Biostatistics, Fred N. Binka School of Public Health, University of Health and Allied Sciences, Hohoe, Ghana

2 Research and Innovation Unit, College of Nursing and Midwifery, Nalerigu, Ghana

Dorcas Serwaa

3 Department of Obstetrics and Gynecology, University of Melbourne, Melbourne, Australia

Alhassan Abdul-Mumin

4 Department of Pediatrics and Child Health, School of Medicine, University for Development Studies, Tamale, Ghana

5 Department of Pediatrics, Tamale Teaching Hospital, Tamale, Ghana

Neonatal jaundice is a common medical condition that affects neonates in the early days of life. Nurses and midwives play important role in the identification and management of neonatal jaundice and the promotion of good neonatal health and education. Their clinical knowledge of neonatal jaundice may influence their attitude and practices toward the identification and management of neonatal jaundice. The study results showed that the level of good knowledge, attitudes, and practices toward neonatal jaundice management was 69.30% (140/202), 64.90% (131/202), and 62.90% (127/202), respectively. The inferential statistics showed a positive association between good knowledge and attitudes toward neonatal jaundice and good practices of neonatal jaundice management. Suggestively, nurses and midwives who have and demonstrate better clinical knowledge and exhibit positive attitudes are more likely to implement appropriate practices for the management of neonatal jaundice. Healthcare providers should therefore invest in life-long learning activities for staff, especially in the study setting.

Introduction

Neonatal jaundice is a common pediatric condition that refers to the yellowish coloration of the skin, sclera of the eye, and other organs of the body caused by the accumulation of bilirubin ( American Academy of Pediatrics et al., 2004 ; Huang et al., 2022 ). It affects nearly 50% to 60% of full-term babies and 80% of premature babies develop jaundice within the first week postdelivery( American Academy of Pediatrics et al., 2004 ; Huang et al., 2022 ). Neonatal jaundice can be a life-threatening condition without the appropriate treatment and management, and has been associated with high rates of disability and mortality ( Amegan-Aho et al., 2019 ; Khan et al., 2015 ). Early detection, timely treatment, and management of neonatal jaundice are important measures to prevent associated complications. As one of the main caregivers, nurses and midwives provide essential care to newborns before discharge from the hospital ( Donkor et al., 2023 ). Nurses and midwives may be the first to observe early signs of jaundice, therefore, having improved knowledge, attitude, and good clinical practices toward neonatal jaundice is central to achieving favorable outcomes for the management of neonatal jaundice. We therefore write a commentary on a recently published paper “Neonatal Jaundice Management: Knowledge, Attitude, and Practice Among Nurses and Midwives in the Northern Region, Ghana” ( Donkor et al., 2023 ), highlighting the study's findings for improved outcomes for the management of neonatal jaundice.

Brief Review

Neonatal jaundice seems to be a common medical condition among newborns in Ghana with an increasing trend. Previous reports from 2015 to 2019 highlight the year-on-year increase. Absolute figures of neonatal jaundice from the year 2015 to 2019 were reported to be 3,031, 4,251, 5,338, 7,175 and 9,273, respectively ( Ghana Health Service, 2019 ; Salia et al., 2021). The epidemiological distribution of neonatal jaundice varies in-country, ranging between 9.7% and 66.7% in the Northern and Central Regions, respectively ( Abdul-Mmumin et al., 2021 ; Adoba et al., 2018 ). Severe form of neonatal jaundice has been reported in some parts of the country ( Adei-Atiemo et al., 2015 ). Neonatal jaundice has been associated with postdelivery hospital readmission ( Seneadza et al., 2022 ). The health threats of neonatal jaundice include kernicterus, hearing loss, cerebral palsy, and death (Mwaniki et al., 2012; Seneadza et al., 2022 ). The health threats of neonatal jaundice highlight the need to address poor clinical knowledge and skills to diagnose and manage the condition effectively.

Current Insights and Interpretations

The study reported a substantial level of good knowledge of 69.30% (140/202) of neonatal jaundice. However, the proportion of participants with poor knowledge 30.70% (62/202) of neonatal jaundice is significant. In the clinical setting, poor knowledge of a condition can lead to misdiagnosis, mistreatment, and poor health outcomes. Participants with poor level of knowledge of neonatal jaundice are placed on duty as those with good knowledge. They are expected to provide the best care to patients. It is therefore important to improve the identified clinical knowledge gap through continuous professional capacity building. The continuous professional capacity building could assume the form of in-service training, expert lecture series, and clinical peer-review sessions. The nurses could equally consult open-source journals and resources to improve their clinical knowledge of neonatal jaundice. Specialization through professional education and training is equally recommended.

Overall, the study reported good attitude and practice of neonatal jaundice to be 64.90% (131/202) and 62.90% (127/202), respectively. The findings are in the regions of 60% with the reported level of knowledge of neonatal jaundice 69.30% (140/202). This observation may highlight the link between clinical knowledge, and attitudes and practices of neonatal jaundice. The inferential statistics of the study emphasized the significant positive association between good knowledge and attitudes toward neonatal jaundice and good practices of neonatal jaundice management. This may be an indication that nurses and midwives who have and demonstrate better clinical knowledge and exhibit positive attitudes are more likely to implement appropriate practices for the management of neonatal jaundice.

Conclusions

Overall, the study showed a substantial level of knowledge, attitudes, and practices of nurses and midwives toward neonatal jaundice management. However, there exist important gaps in the level of knowledge, attitude, and practices toward neonatal jaundice management among participants.

Importance to Nursing Profession

The study stresses the need for continued neonatal jaundice education, training, and support to enhance the nurses’ and midwives’ knowledge and practices that will ultimately benefit neonatal health outcomes. Improving the clinical knowledge of nurses and midwives would have a cascading positive effect on their attitudes and practices toward neonatal jaundice management. Equally extending the study to other settings and multiple health facilities would be valuable to develop national programs on neonatal jaundice. Future studies should focus on clinical assessment and a better appreciation of the burden and epidemiology of neonatal jaundice.

To maximize the importance of the study ( Donkor et al., 2023 ), it is recommended that authors disseminate findings with health facilities in the study area. It is equally important for authors to collaborate with health facilities to develop context-based in-service training manuals on neonatal jaundice for healthcare providers such as nurses and midwives to maximize neonatal health.

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding: The authors received no financial support for the research, authorship, and/or publication of this article.

ORCID iD: Edem Kojo Dzantor https://orcid.org/0000-0002-6195-3898

• Abdul-Mmumin A., Owusu E. A., Mwindekuma P., Tabiri S. (2021). Maternal knowledge and awareness of neonatal jaundice in term neonates admitted to the neonatal intensive care unit of the tamale teaching hospital . Journal of Medical and Biomedical Sciences , 8 , 12–17. [ Google Scholar ]
• Adei-Atiemo E., Rodrigues O., Badoe E. (2015). Classification and risk factors for cerebral palsy in the Korle Bu Teaching Hospital, Accra: A case–control study . Pediatrics , 135 ( Supplement_1 ), S7–S7. 10.1542/peds.2014-3330k [ CrossRef ] [ Google Scholar ]
• Adoba P., Ephraim R. K. D., Kontor K. A., Bentsil J.-J., Adu P., Anderson M., Sakyi S. A., Nsiah P. (2018). Knowledge level and determinants of neonatal jaundice: A cross-sectional study in the Effutu Municipality of Ghana . International Journal of Pediatrics , 2018 , 1–9. 10.1155/2018/3901505 [ PMC free article ] [ PubMed ] [ CrossRef ] [ Google Scholar ]
• Amegan-Aho K. H., Segbefia C. I., Glover N. D. O., Ansa G. A., Afaa T. J. (2019). Neonatal jaundice: Awareness, perception and preventive practices in expectant mothers . Ghana Medical Journal , 53 ( 4 ), 267–272. 10.4314/gmj.v53i4.3 [ PMC free article ] [ PubMed ] [ CrossRef ] [ Google Scholar ]
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• Donkor D. R., Ziblim S. D., Dzantor E. K., Asumah M. N., Abdul-Mumin A. (2023). Neonatal jaundice management:Knowledge, attitude, and practice among nurses and midwives in the Northern Region, Ghana . SAGE Open Nursing , 9 , 1–13. 10.1177/23779608231187236 [ PMC free article ] [ PubMed ] [ CrossRef ] [ Google Scholar ]
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• Huang Y., Chen L., Wang X., Zhao C., Guo Z., Li J., Yang F., Cai W. (2022). Maternal knowledge, attitudes and practices related to neonatal jaundice and associated factors in Shenzhen, China: A facility-based cross-sectional study . BMJ Open , 12 ( 8 ), 1–11. 10.1136/bmjopen-2021-057981 [ PMC free article ] [ PubMed ] [ CrossRef ] [ Google Scholar ]
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• Mwaniki M. K., Atieno M., Lawn J. E., Newton C. R. (2012). Long-term neurodevelopmental outcomes after intrauterine and neonatal insults: A systematic review . Lancet , 379 , 445–452. 10.1016/S0140-6736(11)61577-8 [ PMC free article ] [ PubMed ] [ CrossRef ] [ Google Scholar ]
• Salia, S. M., Afaya, A., Wuni, A., Ayanore, M. A., Salia, E., Kporvi, D. D., Adatara, P., Yakong, V. N., Eduah-Quansah, S. A., Quarshie, S. S., Dey, E. K., Akolga, D. A., & Alhassan, R. K. (2021). Knowledge, attitudes and practices regarding neonatal jaundice among caregivers in a tertiary health facility in Ghana. PloS one , 16 (6), e0251846. 10.1371/journal.pone.0251846 [ PMC free article ] [ PubMed ] [ CrossRef ] [ Google Scholar ]
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Neonatal Jaundice Clinical Case

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Case Presentation Obstructive Jaundice - PowerPoint PPT Presentation

Case Presentation Obstructive Jaundice

Case presentation obstructive jaundice dr. ravi madhusudhana professor dr. manjunath post graduate dept of anaesthesiology. sdumc, kolar. * * * * identification of ... – powerpoint ppt presentation.

• Dr. Ravi Madhusudhana
• Dr. Manjunath
• Post Graduate
• Dept of Anaesthesiology. SDUMC, Kolar.
• History- Relevant To Causes Of Jaundice Symptoms
• Abdominal Examination To Differentiate Liver/ Spleen/Kidney For Ascites
• Types Of Jaundice- LFT
• Problems Of Hyperbilirubinemia
• Relevance Of Child-pugh Score
• Accumulation of Bilirubin (yellow pigment)in the skin and other tissues
• Hemolytic Jaundice
• Hepatic Jaundice
• Obstructive Jaundice(Cholestasis)
• Congenital Jaundice
• It is due to intra- or extra hepatic obstruction of bile ducts
• Intra Hepatic Jaundice
• Primary Biliary Cirrhosis,
• Drugs (contact with DDT, heavy metals, beryllium )
• Extra Hepatic Biliary Obstruction
• Inflammation,
• Tumors, (Ampulla of Vater)
• Name kalyan,
• Age -50yrs ,
• occupation - Farmer
• Main complaints
• Pain in abdomen - 15 days
• Yellowish discoloration of urine - 12 days
• Yellowish discoloration of eye - 10 days
• pain at rt. Upper abdomen which is sudden in onset ,severe and colicky in nature ,increasing intensity for 2-3 min then relieved spontaneously after few minutes.
• Frequency of pain was initially 2-3 times a day, presently 4-6 times a day.
• Pain was non radiating in nature and increases on food intake and pt used to get mild relief on taking analgesic .
• Pain was associated with nausea and vomiting .
• Pain was not associated with body posture
• Pt. also noticed clay colored stool since 12 days with yellowish discoloration of urine which gradually increased in intensity
• No H/O of burning micturition
• Then he also noticed yellowish discoloration of eyes followed by nail and palm.
• Pt. is also giving h/o itching all over body since 8 days which was more in night .
• There is also H/O decreased appetite since 4 days
• Feeling better with less pain jaundice after an endoscopic stenting procedure done 3 days ago
• Negative H/O-
• no H/O fever
• no H/O weight loss
• no H/O similar illness previously
• no history suggestive of
• TB,DM ,HTN, any other chronic illness./ bleeding diathesis
• no H/O blood transfusion / tattoo
• pain, due to
• gallbladder disease,
• malignancy, or
• stretching of the liver capsule
• fever, due to ascending cholangitis
• palpable and / or tender gallbladder
• enlarged liver, usually smooth
• palmar creases, below the breast, on the neck.
• They indicate raised serum cholesterol of several months.
• Xanthomas on the tendon sheaths are uncommonly associated with cholestasis.
• xanthelasma -on the eyelids
• scratch marks excoriation
• finger clubbing
• loose, pale, bulky, offensive stools
• dark orange urine
• Age and sex
• Viral hepatitis is common in young adults.
• CBD stone neoplastic jaundice seen in middle aged or elderly individuals.
• Portal cirrhosis, primary cancer of liver pancreatic cancer predominates in males.
• CBD Stone , PBC, carcinoma gall bladder common in females.
• Any employment involving handling of hepatotoxic agents like
• DDT, heavy metals, beryllium etc should be
• Exposure to infection in medical paramedical workers ,there is a predisposition to leptospirosis among workers in rat infected premises.
• Contact with jaundiced patients, if recent , should suggest possibility of infective hepatitis.
• Family history
• Association with anemia, gall stones removal of spleen suggests hemolytic jaundice.
• Past history
• Recent biliary tract surgery
• History of alcohol intake in cirrhosis.
• Use of drugs such as chlorpromazine, testosterone.
• Sexual orientation
• Diseases associated with male homosexuality
• Onset of jaundice
• Sudden Viral hepatitis, gall stones
• Gradual more likely with cirrhosis,
• pancreatic carcinoma, metastasis.
• Progressive typical of malignant obstruction.
• Fluctuating Stone in CBD, carcinoma
• ampulla of vater or repeated
• hemolytic episodes.
• Strong colicky character suggests gall stones
• Severe boring pain passing through back
• suggests pancreatitis
• In older patients, painless but fluctuating jaundice suggests intermittent obstruction by gall stones or necrotising papillary carcinoma.
• Painless but progressive jaundice is usually due to
• malignant obstruction of CBD.
• Fever chills
• if associated with bacterial viral infection ascending cholangitis.
• Pruritus characteristic of cholestasis.
• Morning anorexia , nausea retching suggests
• alcoholism if symptoms are longstanding.
• Urine dark coloured indicates cholestasis.
• Stools pale stools indicate cholestatic jaundice.
• EXAMINATION
• Conscious cooperative and well oriented to T/P/P
• Avg. built / Avg.nutrition
• Hair normal
• yellowish sclera - tongue dry and yellowish
• Icterus present / no engorged neck vein / no enlarged lymph node / no pallor / no clubbing/no koilonychiya / no cyanosis / no edema
• No general signs of liver cell failure gynecomastia,
• loss axillary hair, spider naevi, clubbing, leukonychia,
• palmar erythema, hepatic flap
• RR- 14/min regular and abdominothoracic
• Pulse-84/min (rt radial pulse), regular ,normal volume ,
• no R-R delay no R-F delay , all peripheral pulses are palpable
• BP- 130/84 (supine) rt arm ,by auscultatory method
• Temp Afebrile
• airway MPII, mouth opening - adequate
• SYSTEMIC EXAMINATION
• No added sounds
• CVS-S1 S2 normal
• ABDOMEN EXAMINATION-
• INSPECTION- Contour normal flat abdomen
• Umbilicus normal in shape and centrally placed.
• scratch mark present on abdomen
• no visible peristalsis seen
• no any scar mark, no dilated vein
• no petechiae ,no ecchymosis
• no abdominal distension
• local temperature normal
• soft abdomen
• no tenderness
• no rebound tenderness
• no localized swelling
• no hepatomegaly
• no splenomegaly
• no palpable gall bladder
• no fluid thrill
• PERCUSSION-
• tympanic note all over abdomen
• liver dullness present and liver span is 13 cm in
• midclavicular line
• no shifting dullness
• AUSCULTATION-
• bowel sound present
• no added sound and bruit present
• No signs of portal hypertension
• SHIFTING DULLNESS
• Before ERCP
• -Total bilirubin level of 26 mg/dL with a conjugated bilirubin of 18 mg/dL (normal level lt 0.7 mg/dl)
• -Total bilirubin level of 8 mg/dL with a conjugated bilirubin of 6.85mg/dl
• Aspartate aminotransferase 220 IU/L
• Alanine aminotransferase 250 IU/L,
• Hemoglobin level of 9 g/dL.
• Albumin 3 g
• CBC Normal limits
• prothrombin time (secs) 45
• Urinalysis positive bilirubin, normal urobilinogen
• 50 yrs male with complaints of pain in right hypochondrium with yellowish discoloration of body associated with itching and clay colored stool without any history of weight loss, fever and chronic alcohol intake .
• Provisional diagnosis obstructive jaundice post- ERCP status
• D/D-choledocholithiasis
• periampullary growth which obstruct
• biliary tract.
• Detection of hepatocellular injury
• Aminotransferases
• Lactate dehydrogenase
• Glutathione-S-transferase
• Assessment of hepatic protein synthesis
• Serum albumin
• Serum globulin
• Prothrombin time
• Detection of cholestatic disorders
• (Indices of obstructed bile flow)
• Alkaline phosphatase
• 5 nucleotidase
• Gamma glutamyl transpeptidase
• Serum bilirubin(lt1mg/dl)
• Quantitative liver tests
• (Indices of hepatic blood flow metabolic capacity)
• Indocyanine green(ICG)
• Obstructive Jaundice
• Lab Findings
• Serum Bilirubin?
• Feceal urobilinogen? (incomplete obstruction)
• Feceal urobilinogen absence (complete obstruction)
• urobilinogenuria is absent in complete obstructive jaundice
• bilirubinuria ?
• cholesterol ?
• Urinary changes
• bilirubin increased
• urobilinogen reduced or absent
• Faecal changes
• stercobilinogen reduced or absent
• ALT/SGPT-cytoplasmic(5-45 IU/L)18 hrs
• AST/SGOT-cytoplasmic and mitochondrial(5-30 IU/L)36 hrs
• Mild(100-249IU/l)- non-specific
• Moderate(250-999IU/l)
• Large(1000-1999IU/l)
• Extreme(gt2000IU/l)
• Mild - steatosis,
• medications,
• alcohol consumption,
• cholestasis, chronic viral hepatitis,
• haemochromatosis, neoplasms, cirrhosis
• Moderate - acute viral hepatitis,
• drug-induced liver injury and
• flare-ups of chronic liver diseases
• Large - acute on chronic active liver disease
• Extreme - fulminant viral hepatitis,
• severe drug induced liver injury,
• shock liver,
• hypoxic hepatitis,
• autoimmune hepatitis,
• acute biliary obstruction
• gt4 wilsons disease
• 2-4 alcoholic liver disease
• lt1 non-alcoholic steatohepatitis
• 105-333 IU/L
• Elevated levels may reflect hepatocellular injury, extrahepatic disorders or both
• Extreme increases signify massive liver disease
• Prolonged concurrent elevations in LDH and AP-malignant infiltration of the liver
• Extrahepatic- hemolysis,
• rhabdomyolysis,
• tumour necrosis,
• renal infarction,
• acute cerebrovascular accident,
• myocardial infarction
• Hepatocellular injury- accompanied by AST/ALT
• Sensitive and specific test for drug induced liver injury
• Serial measurements can reveal the time course of hepatic injury
• In acinar zone 3
• More sensitive than AST or ALT as a marker of centrilobular necrosis in its incipient stages.
• To assess hepatocellular function
• To evaluate chronic liver disease
• Half life of nearly 3 weeks
• Procoagulants have short half life
• Factor VII 4 hrs, fibrinogen 4 days
• Levels descend shortly after liver begins to fail
• PT-measures factors II, V, VII and X
• Prolonged PT- low level of factor VIIa
• 20-140 IU/L(35-115 in males and 25-95 in females)
• Circulating half life 7 days
• To screen diseases of the liver or biliary tree- hepatitis, malignancies and cholestatic diseases
• Extreme increases indicate
• a) major block in biliary flow due to primary biliary
• cirrhosis and choledocholithiasis.
• b) hepatic malignancy compressing some
• intrahepatic bile ducts.
• 5nucleotidase-2-17U/L
• Gamma glutamyl transpeptidase 0-51IU/L(lt70 in males and lt40 in females)
• To distinguish between hepatic and extrahepatic sources of AP
• Changes in AP secondary to hepatobiliary disease usually followed by 5NT
• Serum AP and GGTP increase in tandem, whereas 5NT may not change for days
• Inducible microsomal enzyme( by alcohol, anticonvulsants and warfarin)
• Less specific than 5NT
• Bone contains very little GGTP-therefore distinguish between osseous and hepatobiliary sources.
• Most widely used test for hepatic excretory function
• Normally below 1mg/dl
• gt4mg/dl-yellowish discoloration of body tissues
• Serological testing- viral, microbial and autoimmune
• Genetic testing-heritable metabolic disorders
• Tumor marker assays- hepatic malignancies
• Total Hepatocellular mass- by measuring the clearance of a substance such as indocyanine green, bromsulphalein and rose Bengal
• Drug metabolizing capacity
• Caffeine clearance
• Galactose elimination capacity
• Aminopyrine breath test
• Antipyrine clearance
• Unconjugated bilirubin is toxic for neuronal cell whereas the conjugated bilirubin is responsible for renal dysfunction in patient with obstructive jaundice.
• Bilirubin value rarely exceeds 6mg/dl in Haemolytic anaemia.
• Intrahepatic cholestasis to cause rise in bilirubin, drainage of
• bile in gt75 parenchyma should be blocked
• Sepsis or renal failure should be excluded if the bilirubin exceeds 30mg/dl in patient with CBD stone.
• Serum bilirubin will take atleast 1-2 weeks to return to normal following the relief of obstruction ( half life of bilirubin is 2weeks).
• Negative inotropic effect by bile salt.
• Negative chronotropic effect by bile salt.
• Due to activation of RAS, intravascular interstitial volume expansion occurs, several types of shunts develop ,leading to hyderdynamic circulation.
• Decreased vascular resistance( peripheral vasodilation, increased arteriovenous shunting)
• Blood volume maintained or increased , but redistributed.(splanchnic hypervolaemia, central hypovolemia)
• Increased blood flow in splanchnic (extrahepatic), pulmonary, muscular and cutaneous tissues.
• Decreased total hepatic blood flow
• maintained hepatic arterial blood flow
• decreased portal venous blood flow
• Beta receptor density reactivity in the myocardium of cirrhotic patients diminished, thus ionotropic responses to sympathomimetic drugs reduced in liver disease.
• Intrapulmonary shunting caused by intrapulmonary vascular dilatations(precapillary or arteriovenous)
• triad of chronic liver disease ,increased alveolar
• arterial oxygen gradient and evidence of IPVD is
• defined as hepatopulmonary syndrome.
• Ventilation perfusion mismatch caused by impaired hypoxic pulmonary vasoconstriction, pleural effusions, ascites and diaphragm dysfunction.
• Decrease in pulmonary diffusion capacity secondary to increased extracelluar fluid, interstitial pneumonitis,and/or pulmonary hypertension.
• Haemodynamic instability caused by the bile salts
• endotoxin on the cardiovascular function.
• Three main functional abnormalities in cirrhosis are reduction in sodium excretion,
• reduction in free water clearance,
• decrease in renal perfusion and glomerular filtration.
• Direct nephrotoxic effect by bile salt and conjugated
• bilirubin .
• Renal tubule blockade of bilirubin cast may further
• potentiate the renal injury.
• Decreased production of coagulation and inhibitor factors
• Synthesis of dysfunctional clotting factors
• Quantitative and qualitative platelet defects
• Vitamin K deficiency
• Decreased clearance of activated factors
• Hyperfibrinolysis
• elevated serum bilirubin - in proportion to duration of cholestasis returns to normal once cholestasis is relieved
• raised serum alkaline phosphatase - to more than 3X upper limit of normal
• LFTs - aminotransferases mildly raised raised gamma GT
• increased urinary bilirubin
• urinary urinobilinogen is excreted in proportion to amount of bile reaching the duodenum i.e. absence of urinobilinogen indicates complete biliary obstruction
• The first diagnostic test to use in patients whose liver tests suggest cholestasis,
• To look for the presence of a dilated intrahepatic or extrahepatic biliary tree or to identify gallstones.
• In addition, it shows space-occupying lesions within the liver, enables the clinician to distinguish between cystic and solid masses.
• Ultrasound with Doppler imaging can detect the patency of the portal vein, hepatic artery, and hepatic veins and determine the direction of blood flow.
• Dilated ducts on ultrasound - percutaneous transhepatic cholangiograpy
• Undilated ducts on ultrasound - endoscopic retrograde cholangio-pancreatography
• Needle biopsy of the liver
• Pain, jaundice (charcot s triad)
• Hepatomegaly
• Spleenomegaly
• GI bleeding
• Once Jaundice is recognized, it is important to determine whether hyperbilirubinemia is predominantly Conjugated B or UnConjugated B?
• Differentiation of hemolytic from other type of Jaundice is usually not difficult.
• The laboratory findings are in constant in partial biliary obstruction and differentiation from intrahepatic cholestesis is particularly difficult.
• Jaundice- Differential diagnosis
• Differential Diagnosis
• Exclude UCB (e.g. hemolysis or Gilbert Synd.)
• Distinguish hepatocellular from obstructive
• Distinguish intrahepatic from extra hepatic cholestasis
• DIXON FREIDMAN RISK FACTORS
• S.Bilirubin gt 11mg/dl
• Malignant obstruction
• Haematocrit lt 30
• Renal failure
• Cholangitis
• Hypoalbuminemia
• If at least 3 of above mortality 60
• If none of above mortality 5
• Child A - Safely undergo elective surgery.
• Child B - may undergo elective surgery after
• optimisation with caution.
• Child C - Contraindication for elective surgery.
• Presence of infection
• WBC gt 10,000
• Treatment with gt 2 antibiotics
• PT gt 1.5 sec over control
• Presence of ascites
• Malnutrition
• Emergence surgery

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OBSTRUCTIVE JAUNDICE

May 11, 2012

680 likes | 1.43k Views

OBSTRUCTIVE JAUNDICE. DR.RAMDAS RAI PROF. &amp; UNIT CHIEF YMCH. Definition Epidemiology Classification Pathophysiology Clinical evaluation Management. Outline of Discussion.

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OBSTRUCTIVE JAUNDICE DR.RAMDAS RAI PROF. & UNIT CHIEF YMCH

Definition • Epidemiology • Classification • Pathophysiology • Clinical evaluation • Management Outline of Discussion

Jaundice is the yellowish pigmentation of the skin, the conjunctival membranes over the sclerae, and other mucous membranes caused by hyperbilirubinemia. • Total serum bilirubin values are normally 0.2-1.2 mg/dL. Jaundice may not be clinically recognizable until levels are at least 3 mg/dL. DEFINITION

Jaundice is not a diagnosis. • Surgical jaundice is any jaundice amenable to surgical treatment. Majority are due to extrahepatic biliary obstruction. • Not all obstructive jaundice is surgical jaundice e.g hepatitis and not all surgical jaundice is due to obstruction e.g congenital spherocytosis

RACE • The racial predilection depends on the cause of the biliary obstruction. • Gallstones are the most common cause of biliary obstruction. EPEDEMIOLOGY

Persons of Hispanic origin and Northern Europeans have a higher risk of gallstones compared to people from Asia and Africa. • Native Americans (particularly Pima Indians)have a lifetime chance of developing gallstones as high as 80%.

SEX • Women are much more likely to develop gallstones than men. • This increased risk is likely caused by the effect of estrogen on the liver, causing it to remove more cholesterol from the blood and diverting it into the bile.

To better understand these disorders, a brief discussion of the normal structure and function of the biliary tree is needed. • Bile is the exocrine secretion of the liver and is produced continuously by hepatocytes. It contains cholesterol and waste products, such as bilirubin and bile salts, which aid in the digestion of fats. Half the bile produced runs directly from the liver into the duodenum via a system of ducts, ultimately draining into the common bile duct (CBD). The remaining 50% is stored in the gallbladder. PATHOPHYSIOLOGY

In response to a meal, this bile is released from the gallbladder via the cystic duct, which joins the hepatic ducts from the liver to form the CBD. The CBD courses through the head of the pancreas for approximately 2 cm before passing through the ampulla of Vater into the duodenum

Biliary obstruction refers to the blockage of any duct that carries bile from the liver to the gallbladder(intrahepatic) or from the gallbladder to the small intestine(extrahepatic). • This can occur at various levels within the biliary system.

The major signs and symptoms of biliary obstruction result directly from the failure of bile to reach its proper destination. • The failure of biliary flow may be due to biliary obstruction by mechanical means or by metabolic factors in the hepatic cells.

For the sake of simplicity, the primary focus here will be mechanical causes of biliary obstruction, further separating them into intrahepatic and extrahepatic causes.

Intrahepatic cholestasis generally occurs at the level of the hepatocyte or biliary canalicular membrane. Causes include hepatocellular disease (eg, viral hepatitis, drug-induced hepatitis), drug-induced cholestasis, biliary cirrhosis, and alcoholic liver disease.

In hepatocellular disease, interference in the 3 major steps of bilirubin metabolism, ie, uptake, conjugation, and excretion, usually occurs. Excretion is the rate-limiting step and is usually impaired to the greatest extent. As a result, conjugated bilirubin predominates in the serum

Extrahepaticobstruction to the flow of bile may occur within the ducts or secondary to external compression. Overall, gallstones are the most common cause of biliary obstruction. Other causes of blockage within the ducts include malignancy, infection, and biliary cirrhosis.

External compression of the ducts may occur secondary to inflammation (eg, pancreatitis) and malignancy. Regardless of the cause, the physical obstruction causes a predominantly conjugated hyperbilirubinemia

The lack of bilirubin in the intestinal tract is responsible for the pale stools typically associated with biliary obstruction. • The cause of itching (pruritus) associated with biliary obstruction is not clear. Some believe it may be related to the accumulation of bile acids in the skin. Others suggest it may be related to the release of endogenous opioids.

Causes of biliary obstruction can be separated into intrahepatic and extrahepatic. • Intrahepatic causes are most commonly hepatitis and cirrhosis, Drugs e.g thiazides, chlorpromazine,augmentin etc • Extrahepaticcauses may be further subdivided into intrinsic, intraluminal and extrinsic CAUSES

Stone disease is the most common cause of obstructive jaundice.Larger stones can become lodged in the CBD and cause complete obstruction, with increased intraductal pressure throughout the biliary tree.

Mirizzisyndrome is the presence of a stone impacted in the cystic duct or the gallbladder neck, causing inflammation and external compression of the common hepatic duct and thus biliary obstruction.

Of biliary strictures, 95% are due to surgical trauma and 5% are due to external injury to the abdomen or pancreatitis or erosion of the duct by a gallstone. • A tear in the duct causes bile leakage and predisposes the patient to a localized infection. In turn, this accentuates scar formation and the ultimate development of a fibrous stricture.

Of parasitic causes, adult Ascarislumbricoides can migrate from the intestine up through the bile ducts, thereby obstructing the extrahepatic ducts. • Eggs of certain liver flukes (eg, Clonorchissinensis, Fasciola hepatica) can obstruct the smaller bile ducts within the liver, resulting in intraductal cholestasis. This is more common in Asian countries

Primary Sclerosing Cholangitis is most common in men aged 20-40 years, and the cause is unknown. • Primary Sclerosing Cholangitis is characterized by diffuse inflammation of the biliary tract, causing fibrosis and stricture of the biliary system. It generally manifests as a progressive obstructive jaundice and is most readily diagnosed based on findings from endoscopic retrograde cholangiopancreatography (ERCP).

AIDS-related cholangiopathy manifests as abdominal pain and elevated liver function test , suggesting obstruction. The etiology of this disorder in patients who are HIV-positive is thought to be infectious (cytomegalovirus, Cryptosporidium species, and microsporidia have been implicated). • Direct cholangiography often reveals abnormal findings in the intrahepatic and extrahepatic ducts that may closely resemble Primary Sclerosing Cholangitis.

Biliary tuberculosis is extremely rare. • Histopathologicevidence of caseating granulomatous inflammation with bile cytology revealing M tuberculosis is confirmatory. • Polymerase chain reaction is useful to expedite the diagnosis if biliary tuberculosis is being considered

Biliary obstruction associated with pancreatitis is observed most commonly in patients with dilated pancreatic ducts due to either inflammation with fibrosis of the pancreas or a pseudocyst. • Notably, intravenous feedings predispose patients to bile stasis and a clinical picture of obstructive jaundice. Consider this in the evaluation of biliary obstruction.

Sump syndrome is an uncommon complication of a side-to-side choledochoduodenostomy in which food, stones, or other debris accumulate in the CBD and thereby obstruct normal biliary drainage

History • Examination • Investigations • Treatment Clinical Evaluation

Patients commonly complain of pale stools, dark urine, yellowish discolourationof the eye, and pruritus. • The following considerations are important: • Patients' age • Jaundice (duration ,onset, progression) HISTORY

Associated symptoms:- • the presence of abdominal pain( location and characteristics of the pain) • The presence of systemic symptoms (eg:- fever, weight loss) • Symptoms of gastric stasis (eg:- early satiety, vomiting, belching) • Change in bowel habit: • History of anemia

Previous malignancy • Known gallstone disease • Gastrointestinal bleeding • Hepatitis • Previous biliary surgery • Diabetes or diarrhea of recent onset • Also, explore the use of alcohol, drugs, and medications

Upon physical examination, the patient may display signs of jaundice (sclera icterus). • When the abdomen is examined, the gallbladder may be palpable (Courvoisier sign). This may be associated with underlying pancreatic malignancy. PHYSICAL EXAMINATION

COURVOISIER’S LAW:- “When the gallbladder is palpable & the patient is jaundiced , the obstruction of bile duct causing the jaundice is unlikely to be a stone because previous inflammation will have made the gallbladder thick & nondistensible”

Also, look for signs of weight loss, adenopathies, and occult blood in the stool, suggesting a neoplastic lesion. • Note the presence or absence of ascites and collateral circulation associated with cirrhosis. • A high fever and chills suggest a coexisting cholangitis.

Abdominal pain may be misleading; some patients with CBD calculi have painless jaundice, whereas some patients with hepatitis have distressing pain in the right upper quadrant. Malignancy is more commonly associated with the absence of pain and tenderness during the physical examination. • Xanthomata are associated with Primary Biliary Cirrhosis . • Excoriations suggest prolonged cholestasis or high-grade biliary obstruction

Basic • Complete blood count : • Urine analysis : bilirubin present, urobilinogen absent • Stool for ocult blood: Ca ampula • Stool for ova and parasites • Clotting profile: PT deranged • Hepatitis serology: HbsAg, HCV • LFT: LABORATORY TESTS pptk

Plain radiographs are of limited utility to help detect abnormalities in the biliary system • Ultrasonography (USG):USG is the procedure of choice for the initial evaluation of cholestasis and for helping differentiate extrahepatic from intrahepatic causes of jaundice. Extrahepatic obstruction is suggested by the presence of dilated bile ducts, but the presence of normal bile ducts does not exclude obstruction that may be new or intermittent. IMAGING

Traditional Computed Tomography (CT) scan is usually considered more accurate than USG for helping determine the specific cause and level of obstruction. • Percutaneous transhepaticcholangiogram: done espesciallyif the intrahepatic duct is dilated, outline the biliary tree, locates stones and is therapeutic for stent placement and stone retrieval.

ERCP is an outpatient procedure that combines endoscopic and radiologic modalities to visualize both the biliary and pancreatic duct systems. • Endoscopic ultrasound (EUS) combines endoscopy and USG to provide remarkably detailed images of the pancreas and biliary tree. It uses higher-frequency ultrasonic waves compared to traditional USG (3.5 MHz vs 20 MHz) and allows diagnostic tissue sampling via EUS-guided fine-needle aspiration (EUS-FNA)

Magnetic resonance cholangiopancreatography (MRCP) is a noninvasive way to visualize the hepatobiliary tree. • MRCP provides a sensitive noninvasive method of detecting biliary and pancreatic duct stones, strictures, or dilatations within the biliary system. It is also sensitive for helping detect cancer.

Medical care:Treatment of the underlying cause is the objective of the medical treatment of biliary obstruction. Do not subject patients to surgery until the diagnosis is clear. • In cases of cholelithiasis in which either the patient refuses surgery or surgical intervention is not appropriate give Treatment

Ursodeoxycholic acid (10 mg/kg/d) works to reduce biliary secretion of cholesterol. In turn, this decreases the cholesterol saturation of bile. • Extracorporeal shock-wave lithotripsy may be used as an adjunct to oral dissolution therapy. By increasing the surface-to-volume ratio of the stones, it both enhances dissolution of stones and makes clearing the smaller fragments easier. • Contraindications include complications of gallstone disease (eg, cholecystitis, choledocholelithiasis, biliary pancreatitis), pregnancy, and coagulopathy or anticoagulant medications (ie, because of the risk of hematoma formation).

Bile acid–binding resins, cholestyramine (4 g) or colestipol (5 g), dissolved in water or juice 3 times a day may be useful in the symptomatic treatment of pruritus associated with biliary obstruction. • VIT ADEK SUPPLEMENTS • Antihistamines may be used for the symptomatic treatment of pruritus, particularly as a sedative at night.

Discontinuation of medications that may be causing or exacerbating cholestasis and/or biliary obstruction often leads to full recovery. Similarly, appropriate treatment of infections (eg, viral, bacterial, parasitic) is indicated.

The following are problems of a jaundiced patient and all must be taken care of before surgery • Infection due to biliary stasis • Uncontrolled bleeding due to vit k deficiency • Liver glycogen depletion • Dehydration • Hepatorenal syndrome SURGERY..Preop care

Fluid resuscitation using dextrose alternate with Saline. Encourage oral rehydration as well • Give broad spectrum antibiotics at induction of anaesthesia to cover for Gram+,Gram- and anaerobes • Bowel preparation • Inj.VitK10mg IM daily until PT INR normalises( start 5 days preoperatively) • Monitor urine output • You may consider giving mannitol preoperative ,intraopand post op for diuresis to prevent hepatorenal syndrome Therefore;

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OBSTRUCTIVE JAUNDICE. PROF P DARWIN PROF AND HEAD DEPT OF GENERAL SURGERY STANLEY MEDICAL COLLEGE. WHAT IS JAUNDICE ?. Yellowish pigmentation of the conjunctival membranes over the sclerae and other mucous membranes caused by increased levels of bilirubin in the blood &gt;2 mg/dl.

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Obstructive jaundice for 3 mon with itching &amp; wt.loss

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Jaundice is the yellowish staining of the skin and the whites of the eyes that is caused by high levels of the chemical bilirubin in blood. Jaundice. Very common in babies. Treatment for babies with Jaundice.

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Obstructive Jaundice: A rare cause

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Jaundice. Dr. Ahmed Kensarah. Introduction.

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Jaundice. Definition Accumulation of yellow pigment in the skin and other tissues (Bilirubin). Bilirubin Metabolism Bilirubin formation Transport of bilirubin in plasma Hepatic bilirubin transport Hepatic uptake Conjugation Biliary excretion Enterohepatic circulation. Iron hemoglobin

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OBSTRUCTIVE JAUNDICE. Presented by: MD. TANVIR MAJUMDER, Roll no.144 MD. MAHEDI HASAN, Roll no.150 MONIRUL HOQUE, Roll no.162 MD. SHAHADATH HOSSAIN, Roll no.163. CASE PRESENTATION ON: Obstructive jaundice. PARTICULARS OF THE PATIENT :.

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JAUNDICE. Ultrasound Obstructive Hepatocellular. Obstructive Jaundice. Gallstones Pancreatic Cancer Cholangiocarcinoma Ampullary tumour Benign Biliary stricture Metastatic-Liver, Portal Primary sclerosing cholangitis IgG 4 disease Surgical trauma. ERCP or PTC.

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Jaundice. Mohammed Al- Rajeh &amp; Shreef Al- Qahtani. Anatomy of Biliary Tract. Conditions of the gallbladder &amp; billiary tree. Colelithiasis : Stones in the gallbladder ( 85% cholesterol, 15% pigmented). Male : Female ratio (1:2 ). INCIDENCE: 10% Signs &amp; Symptoms : Asymptomatic

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RT.hypochondrial pain , obstructive jaundice and vomting 2 wk duration.

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Jaundice. Cyanosis. Vitiligo. Albinism. Bullae. Desquamation. Macule. Nodule. Papules. Pustules. Vesicles. Wheals. Crusts. Furuncle. Carbuncle. Urticaria. Eczema. Excoriation.

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Jaundice. Approach to the Jaundiced Infant.

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