How Common Are Cerebrospinal Fluid Leaks After Minor Head Trauma?

Patient Presentation
A 7-year-old male came to clinic for follow up after tripping and falling 6 days previously. He had hit his face on a table and then on the floor sustaining a contusion above his left eyebrow and having epistaxis. He denied any loss of consciousness or emesis. The epistaxis was controlled within 10 minutes and he was seen at a local emergency room, where he was found to have a small contusion, no nasal fracture or septal hematoma. He had a small blood clot on the lateral area of his nostril. Mental status, dental and neck examinations were reportedly normal. His mother said that in the evening he had a headache but had not had any others. She noted that he been doing his regular activities but was significantly more tired in the evenings and went to bed early. He reported no sleep disturbance or nausea, nor difficulties in speaking, talking or thinking. It was not taking him longer to do his work at school and he was able to play on the playground. His mother had kept him out of gym class. His mother noted that the contusion was improving and that he had expelled a small clot from his nose without additional bleeding, but had noted a small amount of rhinorrhea for a couple of days after the clot was expelled. She was concerned because she was a neurosurgical nurse and was worried about cerebrospinal fluid leaking. The rhinorrhea was not continuous and she had only noticed it a few times, with none in the past 1-2 days. The patient did not notice it. They denied any coughing or seasonal allergic rhinitis. The past medical history was notable for excessive cerumen that required intermittent debridement.

The pertinent physical exam showed a well-appearing male in no distress with normal vital signs. HEENT showed a tiny healing contusion above the left eyebrow. No other facial abnormalities were seen. His nasal examination showed no rhinorrhea, hematoma or bleeding. His pharynx was negative. His ears were blocked with cerumen. His neurological examination was negative.

The diagnosis of a healing facial contusion along with probably mild concussion was made. His mother was counseled that although the patient seemed to be doing well at school, that the excessive tiredness was probably due to mild concussion. The physician recommended additional brain rest for a couple of days over the weekend and then to monitor the patient once he resumed his normal activities. “I can understand why you would be concerned about the rhinorrhea but this is more likely due to his nose making some additional fluid to keep the area clean or that he could have had a cold. He didn’t have a nasal fracture, plus it was a low-velocity fall so it would be really unusual for this to be a facial or skull fracture causing a CSF leak,” the physician said. Two days later the boy was seen by otolaryngology for his regularly scheduled followup. They found normal nasal structures and no rhinorrhea.

Discussion
Basilar skulls fractures are relatively common occurring in 4-20% of all skull fractures. Motor vehicle accidents, significant falls from heights and blunt trauma are the most common causes of basilar skull fractures. Basilar skulls fractures are even less common in children than adults. Complications can include meningitis, cerebrospinal fluid (CSF) leaks, cranial nerve injuries or even potentially death. With more significant trauma to the head and body, it is not surprising that complications are more likely.

Nasoethmoid facial fractures have similar common mechanisms of injury including motor vehicle accident, falls, and pedestrian struck injuries.

A review of the timing for concussion symptom resolution can be found here.

Learning Point
CSF leaks can present as otorrhea or rhinorrhea with a basilar skull fracture. Most leaks occur within 48 hours of trauma and most stop without specific treatment usually within a couple of days. A study of hospitalized patients with isolated basilar skull fracture using hospital diagnosis data (N=3563 pediatric patients) found that rates were 2.3% for CSF leaks and 0.48% meningitis respectively.

In a long-term follow up study of post-traumatic basilar skull fractures in hospitalized children (N=196), 28% had CSF leak with 23% having rhinorrhea, and 89% of those stopped spontaneously. Those that didn’t had complicated presentations and courses. The authors state that for children with normal mentation, neurological examination and CT imaging findings in the emergency room after blunt head trauma, that basilar skull fractures have a low-risk of complications and patients can be discharged with outpatient followup.

For CSF leaks that do not spontaneously resolve, patients may be tried on medication that inhibits CSF production such as acetazolamide, and may have an external CSF drainage device placed. Surgical treatment is usually reserved for those with persistent leads more than 10-14 days or with complications.

In a study of 63 pediatric patients, the authors noted that nasoethmoid factures are uncommon fractures, that more simple fractures are often treated without surgical intervention and while complications can occur, they are usually in patients with more severe or multiple injuries. CSF leaking was not reported.

While it is true that any complication can occur in any patient, the patient above had a low-velocity injury, no nasal fracture or other known facial or skull fracture, or other major injury, and the rhinorrhea started several days after the event all of which are less common attributes for CSF leak. Additionally, most CSF leaks spontaneously resolve, therefore continued conservative management and observation was appropriate.

Questions for Further Discussion
1. After a concussion when can a child return to learning? A review can be found here.
2. What are indications for head computed tomography in head trauma?
3. How common are anatomical CSF leaks?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.
Information prescriptions for patients can be found at MedlinePlus for these topics: https://medlineplus.gov/concussion.html and Head Injuries.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Yilmazlar S, Arslan E, Kocaeli H, Dogan S, Aksoy K, Korfali E, Doygun M.
Cerebrospinal fluid leakage complicating skull base fractures: analysis of 81 cases.
Neurosurg Rev. 2006 Jan;29(1):64-71.

McCutcheon BA, Orosco RK, Chang DC, Salazar FR, Talamini MA, Maturo S, Magit A.
Outcomes of isolated basilar skull fracture: readmission, meningitis, and cerebrospinal fluid leak. Otolaryngol Head Neck Surg. 2013 Dec;149(6):931-9.

Leibu S, Rosenthal G, Shoshan Y, Benifla M.
Clinical Significance of Long-Term Follow-Up of Children with Posttraumatic Skull Base Fracture.
World Neurosurg. 2017 Jul;103:315-321.

Lopez J, Luck JD, Faateh M, Macmillan A, Yang R, Siegel G, Susarla SM, Wang H, Nam AJ, Milton J, Grant MP, Redett R, Tufaro AP, Kumar AR, Manson PN, Dorafshar AH. Pediatric Nasoorbitoethmoid Fractures: Cause, Classification, and Management.
Plast Reconstr Surg. 2019 Jan;143(1):211-222.

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

What Are Common Presentations for Budd-Chairi in Adolescents?

Patient Presentation
A 17-year-old female came to clinic for followup from an emergency department visit for abdominal pain 1 week previously. She described abdominal pain in the mid- to upper- quadrants that occurred more in the evening and also during the night. It was described as a 6-7/10 in intensity without radiation and lasted from 5-30 minutes. She describes normal bowel and urinary patterns. She had nausea with the episodes but not at other times and had no emesis. It was not worse with eating, and no foods in particular bothered her.

The past medical history was positive for intermittent abdominal pain for the preceding year. The family history was non-contributory. The review of systems was negative including fever, chills, joint pain, rashes, jaundice, or pruritus. She did have a reported 15 pound weight loss over 2-3 months, with a confirmed 2 pound weight loss since the emergency room visit. She also described just being more tired overall.

The pertinent physical exam showed a thin, tired-appearing female with normal vital signs. Her abdominal examination revealed a slightly protuberant abdomen without a fluid wave. Her liver was palpable ~6 cm below the costal margin and had mild tenderness over it. Her spleen could be palpated also. She had no other tenderness or masses palpable. She had no jaundice but did have prominent veins on her abdomen. Her heart examination was normal without jugular venous distention.

The diagnosis of abdominal pain with hepatosplenomegaly was made.
The radiologic evaluation included an ultrasound of her abdomen which found splenomegaly and hepatomegaly with an undefined area of the right liver lobe that appeared probably vascular. The laboratory evaluation showed elevated liver function tests (ALT = 189 U/L, AST = 208 U/L, total bilirubin = 5.4 mg/dl, with a direct bilirubin of 0.6 mg/dl) with normal prothrombin and INR. Pancreatic and kidney functions along with other chemistries were within normal limits. Urinalysis was normal. The pediatrician contacted the gastroenterology service who saw her the following day and admitted her for further evaluation.

The patient’s clinical course over the next several days included a computed tomographic evaluation which showed a diagnosis of Budd-Chiari syndrome. Evaluations were begun to identify the cause and she was treated medically. She was discharged home and was being monitored closely.

Discussion
Budd-Chiari syndrome (BCS) is a rare liver disease caused by hepatic venous outflow obstruction (HVOTO). The obstruction can be anywhere from the small intrahepatic veins up to the inferior vena cava junction with the right atrium. The liver parenchyma itself is not directly affected but becomes compromised because of the increased hepatic sinusoidal pressure over time. The causes include: prothrombic events (35% of cases such as Protein C or Protein S deficiency, Factor V Leiden or antithrombin deficiency), myeloproliferative conditions, oral contraceptive use, and local factors.

BCS can occur in any age but is more common in the adult population with it occurring more commonly in females than males. Clinically the presentation can be acute, subacute or chronic. Some patients remain asymptomatic (up to 15%) and others present in fulminant hepatic failure. It is believed this is due to the rapidity of the hepatic vein occlusion and the inability to develop collateral circulation. Classically BCS presents as abdominal pain, hepatomegaly and ascites in adult patients. Fever, esophageal bleeding or hepatic encephalopathy are much less common.

Clinical presentation does not correlate with duration of disease. Asymptomatic patients have a good prognosis but symptomatic patients often don’t without treatment. “The reported life expectancy in these patient is 3 years after the first symptoms.” However treatment for underlying causes, angioplasty, transjugular intrahepatic portosystemic shunt (TIPS) procedure and liver transplantation has increased the 5-year survival to 85%.

Diagnosis should be considered with acute or chronic liver disease and is diagnosed by lab testing and imaging.

Learning Point

In a case series of 7 children with BCS, the most common symptoms were abdominal distension, lethargy and anorexia, with abdominal pain being present in only 2 patients. Six patients survived.

In another 6-year case series of 25 children and adolescents with BCS, the most common presenting symptoms were abdominal distension (N=20), loose stools (N-8), with other problems such as poor feeding, fever, edema, abdominal pain, or emesis all occurring in 2 patients or fewer. Seventeen patients were alive at the end of the series.

In a third study of 43 adolescents with BCS who were compared to adult and children, hepatomegaly without ascites was more common in adolescents than adults or children (14/43). Thrombophilic causes were less common for the adolescents than adults but similar to children. They found that 10% of adult patients had their first symptoms in adolescence. They also found an improved response to therapy for adolescents (particularly medical therapy) and believe this may be because of increased collateral vascular formation. Four adolescents died compared to 12/129 adults.

“It may be argued that the disease course of BCS may have its origin in adolescence in a subset of adult patients…[t]he more severe symptoms of adult patient might have resulted from delayed diagnosis and treatment or milder symptoms of adolescent patients due to early diagnosis and treatment.”

Questions for Further Discussion
1. What causes abdominal distension? A review can be found here
2. What causes an abdominal mass? A review can be found here

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.
Information prescriptions for patients can be found at MedlinePlus for this topic: Liver Diseases

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Nobre S, Khanna R, Bab N, Kyrana E, Height S, Karani J, Kane P, Heaton N, Dhawan A. Primary Budd-Chiari Syndrome in Children: King’s College Hospital Experience. J Pediatr Gastroenterol Nutr. 2017 Jul;65(1):93-96.

Valla DC. Budd-Chiari syndrome/hepatic venous outflow tract obstruction. Hepatol Int. 2018 Feb;12(Suppl 1):168-180.

Redkar R, Bangar A, Hathiramani V, Raj V, Swathi C. Pediatric Budd-Chiari Syndrome: A Case Series. Indian Pediatr. 2018 Oct 15;55(10):871-873.

Shukla A, Bhatt P, Gupta DK, Modi T, Patel J, Gupte A, Meshram M, Bhatia S. Budd-Chiari syndrome has different presentations and disease severity during adolescence. Hepatol Int. 2018 Nov;12(6):560-566.

Raza SM, Zainab S, Shamsaeefar AR, Nikeghbalian S, Malek Hosseini SA. Experience of Liver Transplant in Patients Diagnosed with Budd-Chiari Syndrome. Exp Clin Transplant. 2018 Apr;16(2):177-181.

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

What is This Itchy Rash?

Patient Presentation
A 12-year-old African-American female came to clinic with a new rash for 2-3 weeks that was intensely pruritic. It was mainly truncal and general lotion applications had not improved her symptoms. Her sleep had been disturbed because of the pruritus and she was now taking diphenhydramine at night. She denied any new soaps, lotions, cosmetics, detergents, insect repellent, sun creams, etc. She also denied any travel, sleeping in others beds, or trying on other people’s clothes or clothing at a store, or furry animal contact. No one else in the household or friends had any similar symptoms.

The past medical history was positive for moderate intermittent asthma when she was younger, but in the past couple of years she was not having any symptoms. The family history was positive for asthma, allergic rhinitis, diabetes and heart disease. The review of systems was otherwise negative.

The pertinent physical exam showed a healthy female with normal vital signs and growth patterns. Her skin reveals a red, extensive, papular rash over her entire trunk, to her hair line, down the top part of her arms and legs, with sparing of the axillary and groin areas. There was no scale or umbilication. There were extensive excoriations but no areas looked to have secondary infection. There was no hypo- or hyper-pigmentation.

The pediatrician was uncertain of the diagnosis and considered scabies because of the intense pruritus but the distribution was not classic and given the time frame it probably would have spread to some of the usual areas. Atopic dermatitis was also considered but there appeared to be little xerosis. Gianotti Crosti was considered too but again the distribution was not appropriate. Contact dermatitis also seemed unlikely. Pictures were taken and dermatology was contacted who made the diagnosisof follicular eczema and prescribed steroid creams and consistent emollient application.
No followup was available.

Discussion
Atopic dermatitis (AD) has a prevalence of 3-5% in the overall U.S. population but is increasing with an estimated 10-15% lifetime risk in childhood. It is even more common in children of color with a prevalence in African-American/black children of 17% and Hispanic children of 14%. Health care utilization data also appears to support more severe disease in children of color also.

Atopic dermatitis or eczema is a common dermatological skin problem which characteristically is a pruritic, papular eruption with erythema. Like most papulosquamous eruptions it often occurs in intertrigenous areas in people with allergic constitutions or with a family history of atopy. Sometimes atopic dermatitis is described as the “itch that rashes.” Rubbing and scratching can lead to excoriation and, over time, lichenification. There can also be secondary infections or changes to the skin pigmentation (hyper- or hypo-) in affected areas. AD does not have scale which occurs in other papulosquamous eruptions such as psoriasis or tinea. Emollients for skin rehydration are a mainstay of treatment. Topical steroids are commonly used to decrease inflammation in affected areas. Immunosuppressants such as tacrolimus are also used in some cases.

Common differential diagnoses include contact dermatitis, keratosis pilaris, nummerular dermatitis, psoriasis, scabies, seborrhea and tinea corporis, but others can also be considered depending on age and circumstances. A more extensive differential diagnosis of AD can be found here. More information about scabies can be found here. Information about Gianotti Crosti can be found here.

For pathologists, a skin biopsy will show spongiosis or intracellular edema in the epidermis with the desmosome junctions being easy to identify. Other classical changes including infiltration with various cells helps to classify typical patterns and specific diagnoses. With atopic dermatitis for example, dermal eosinophils are commonly seen.

Learning Point
Follicular atopic dermatitis is very common in persons of color, particularly African-American, Asian and Hispanic patients. Patients and parents often report severe pruritus but without the eczematous changes. However there is follicular prominence on the trunk and proximal extremities. Mid- to high-potency steroid creams along with emollients usually work in 2-4 weeks. Anti-histamines are often necessary because of the severe pruritus.

AD is known to have genetic variants associated with it. Unsurprisingly, these appear to be different for different populations, and unfortunately large scale genetic data sets have limited representation of African-Americans.

In skin of color, follicular accentuation and lichenification, hyper- or hypo-pigmentation are more common. Prurigo lesions (e.g. itchy nodules) are also more common in skin of color.

In a study of race and dermatological conditions presenting to a general outpatient dermatology clinic, the most common problems were:

  • White/caucasian = benign skin neoplasm (22%), eczema or dermatitis (13%), adnexal disease (11%)
  • African American/black = eczema or dermatitis (22%), adnexal disease (16%), follicular disorders (10%)
  • Asian = eczema or dermatitis (25%), adnexal disease (13%), benign skin neoplasm (12%)
  • Native American = eczema or dermatitis (17%), benign skin neoplasm (17%), adnexal disease (13%)
  • Multiracial = eczema or dermatitis (24%), adnexal disease (17%), benign skin neoplasm (9%)

Eczema or dermatitis included atopic dermatitis, contact or irritant allergy, and nummular dermatitis.

Questions for Further Discussion
1. What are indications for referral to a dermatologist?
2. What are indications for use of a topical steroid cream?

3. What other dermatological problems are more common or severe in persons of color?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for this topic: Eczema

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Sardana K, Arora P, Mishra D. Follicular eczema: a commonly misdiagnosed dermatosis. Indian Pediatr. 2012 Jul;49(7):599.

Fischer AH, Shin DB, Margolis DJ, Takeshita J. Racial and ethnic differences in health care utilization for childhood eczema: An analysis of the 2001-2013 Medical Expenditure Panel Surveys. J Am Acad Dermatol. 2017 Dec;77(6):1060-1067.

Eichenfield LF, Stein Gold LF. Practical strategies for the diagnosis and assessment of atopic dermatitis. Semin Cutan Med Surg. 2017 Mar;36(2 Suppl 2):S36-S38.

Silverberg NB. Typical and atypical clinical appearance of atopic dermatitis. Clin Dermatol. 2017 Jul – Aug;35(4):354-359.

Gaulding JV, Gutierrez D, Bhatia BK, Han X, Krajenta R, Neslund-Dudas C, Lim HW, Pritchett EN. Epidemiology of Skin Diseases in a Diverse Patient Population. J Drugs Dermatol. 2018 Oct 1;17(10):1032-1036.

Daya M, Barnes KC. African American ancestry contribution to asthma and atopic dermatitis. Ann Allergy Asthma Immunol. 2019 Feb 15. pii: S1081-1206(19)30101-2.

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

What Infectious Diseases are Important to Consider in Transplantation Patients?

Patient Presentation
A 7-year-old male came to clinic to establish care. He and his family had moved to the area for specialty care after he had increasing problems due to hepatic failure secondary to an inborn error of metabolism. He was mainly managed by the regional children’s hospital gastroenterology department, who had referred the family to the transplantation service.

The past medical history was positive for an inborn error of metabolism which caused hepatic failure, short stature, lack of normal growth and development and intellectual disability. The social history showed that the family had extended family in the area and felt that living closer to the hospital would be better for him and for the family in general.

The pertinent physical exam showed a very thin male. His height and weight were 50% for a 4 year old. He seemed happy but with delayed speech and play. The pediatrician estimated his development at around 5 years old. He had yellowed skin with prominent veins on his abdomen. He had a significantly prominent abdomen with a liver that was 6 inches below the ribs and crossed the midline and was very firm. It was difficult to discern other organomegaly or masses because of incooperation. The rest of his examination was essentially normal.

The diagnosis of a new patient who was to have a liver transplant was made. The pediatrician discussed how the practice worked so the family would know how to contact them. “We can help you with any of the lab testing and vaccines. We can also help you when he gets sick which he will just like every other kid. We’ll try to help the transplantation doctors with anything they need. I think most importantly, you should just know that we are here to help you and your child, so just ask us,” she explained.

Discussion
Transplantation is not a common problem for primary care physicians but when a child’s disease has progressed to end-stage organ failure, transplantation can be the only treatment available. While the primary care provider usually is not involved in the daily management of patients before, during and after transplantation, they can be involved in many areas. These can include providing appropriate primary and acute care, ordering and obtaining necessary medical tests, medications and equipment, assisting with medical insurance, providing medical history and records to consultants, translating medical information for the family, general patient and family support, and encouraging and facilitating medical adherence. Pediatricians may have many questions regarding the primary care of a child with a transplant including: What affects the child’s growth?, How efficacious are vaccines after transplant?, What are the outcomes for children with additional problems such as intellectual disability?, and What are the rates of adherence to medical treatment?

There are multiple factors that affect a child’s growth after transplantation including:

  • Type of organ transplanted
  • Patient age at transplant
  • Transplant function
  • Height/weight status pre-transplantation
  • Pubertal stage
  • Medications – particularly corticosteroids

A 2017 systemic analysis of use of corticosteroids, found early withdrawal or avoidance protocols significantly improve final adult height in patients with renal transplantation. Not surprisingly, pre-pubertal patients had the greatest benefit. Use of growth hormone also can increase adult height in patients with renal transplantation. Transplantation function or rejection was also unchanged despite less corticosteroid use. For liver transplantation, reduced corticosteroid exposure did not improve final height, but there were only two studies with small numbers of patients who were followed for a shorter time period than the renal transplantation patients which may account for the differences based on transplanted organ.

A 2017 systematic review was performed of live virus vaccinations on immunosuppressed patients due to solid organ or bone-marrow transplantation. There were 339 patients with solid-organ transplantation who received 424 vaccine doses primarily of Measles, Mumps and Rubella, and Varicella vaccines. For solid organ transplantation only 3 individuals had rejection during the study period. One occurred 3 weeks after measles immunization. One had chronic rejection at the time of vaccination and still had chronic rejection 1 year later. One had a single rejection episode more than 1 year after varicella vaccine which was considered unrelated to the vaccine. For solid organ transplantation, seroconversion rates for varicella vaccine range from 25-87%. Even high seroconversion rates have been reported with additional booster vaccinations.

In a 2017 commentary, the authors compiled a table from 18 studies of 1041 patients who had an intellectual disability and received a solid organ transplant. Graft survival was 80-100% with followup 3 months – 9 years (most common length of followup was 3-5 years). Patient survival was 75-100% again over similar time frames.

Adherence to medical treatment particularly pharmacological immunosuppression is extremely important for long-term function of any transplantation including solid organ transplantation. Overall adherence in pediatric solid organ transplantation is 30-76% with nonadherence peaking in the adolescent age range. “Only a minority of patients openly refuse to take their medications. A more common and a harder situation to diagnose, is that where adherence is intermittent. Those patients are often in denial and overestimate their compliance. The consequence and graft function can be smoldering for a long time and go undetected, failing to raise alert signs to patients and their treating teams. Importantly as we do not know what we cannot measure, the extent of non adherence problem is likely underrecognized.” Non adherence can lead to difficulties in transitioning teens and young adults to adult health care providers. (For a review of transitioning care, click here).

Learning Point
Communication between specialist transplant physicians and primary care physicians regarding infectious disease risks before and after transplantation is especially important. Specialists need to learn from the primary care physician which infectious disease risks the patient may be at risk for based on the history. After transplant, children continue to have fevers, coughs, emesis, diarrhea, rashes and pain like any other child which the primary care physician is asked to determine if this is a common illness or potentially a more serious illness or complication.

Infectious diseases that are important at various stages of transplantation include:

  • Pretransplant recipient – undiagnosed or latent infections
    • Cytomegalovirus
    • Epstein-Barr virus
    • Herpes simplex
    • Human immunodeficiency virus
    • Hepatitis B
    • Hepatitis C
    • Syphilis
    • Travel exposures
      • Toxoplasmosis
      • Strongylodiasis
      • Trypanosoma cruzi (Chagas’ Disease)
      • Mycoses (e.g. Blastomycosis, Coccidioidomycosis, Histoplasmosis)
      • Tuberculosis
      • West Nile virus
      • Zika virus
    • Colonization
      • Methicillin-resistant Staphylococcus aureus
      • Vancomycin-resistant enterococcus

    Note that these infections may not necessarily disqualify a patient from receiving a transplantation but may be important to be aware of for overall treatment.
    Screening for colonization is more controversial than screening for undiagnosed, latent or travel exposures.
    Patients should receive vaccination before transplantation if possible.

  • Pretransplantation – Donor
    • Drug resistant bacteria
    • Human immunodeficiency virus
    • Hepatitis B
    • Hepatitis C
    • Syphilis
    • Tuberculosis
    • Mycoses (rare)
    • Other rare pathogens (e.g. Chagas’ disease, Zika virus)

    Note again that these infections in the donor may not disqualify a patient from receiving a transplantation but may be important to be aware of for the overall treatment.

  • Peritransplant/surgical related infections
    • Surgical site infections with appropriate site organisms
      • Heart transplant – sternal infection with Staphylococcus aureus
      • Lung transplant – pneumonia with respiratory pathogens
      • Liver transplant – skin and gastrointestinal flora (e.g. gram- positive and gram-negative bacteria, anaerobes)
      • Renal transplant – urinary tract infection (e.g. Enterococcus and gram-negative uropathogens)
  • Post transplant infections
    • Drug resistant bacteria
    • Clostridium difficile
    • Cytomegalovirus
    • Epstein Barr virus

Questions for Further Discussion
1. What does the liver do? A review can be found here.
2. What are common inborn errors of metabolism?

3. How do various solid organ transplantations differ from each other? i.e. heart vs lung vs liver vs kidney vs bowel

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for these topics: Organ Transplantation and Liver Transplantation.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Croce E, Hatz C, Jonker EF, Visser LG, Jaeger VK, Buhler S. Safety of live vaccinations on immunosuppressive therapy in patients with immune-mediated inflammatory diseases, solid organ transplantation or after bone-marrow transplantation – A systematic review of randomized trials, observational studies and case reports. Vaccine. 2017 Mar 1;35(9):1216-1226.

Yazigi NA. Adherence and the pediatric transplant patient. Semin Pediatr Surg. 2017 Aug;26(4):267-271.

Knackstedt ED, Danziger-Isakov L. Infections in pediatric solid-organ transplant recipients. Semin Pediatr Surg. 2017 Aug;26(4):199-205.

Tsampalieros A, Knoll GA, Molnar AO, Fergusson N, Fergusson DA. Corticosteroid Use and Growth After Pediatric Solid Organ Transplantation: A Systematic Review and Meta-Analysis. Transplantation. 2017 Apr;101(4):694-703.

Wightman A, Diekema D, Goldberg A. Consideration of children with intellectual disability as candidates for solid organ transplantation-A practice in evolution. Pediatr Transplant. 2018 Feb;22(1).

Author
Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa