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Active Cases
Comments are accepted only from Anesthesiology - includes all Subspecialties experts.
66 year old women with significant comorbidities including prior heart infarct and lung process, dies during non-emergent exploratory laparoscopy for bowel obstruction.
Case Overview
Location: CA
66 years old, Female
Past Medical History:
HTN, Other heart conditions, diabetes, ulcerative colitis, hyperlipidemia, atherosclerotic disease, abdominal adhesions
Past Surgical History:
galbladder surgery, hysterectomy, prior bowel obstruction
66 year old female presented to the ED on January 13, 2023 with sharp lower abdominal pain, nausea, and vomiting similar to when she had a small bowel obstruction in 2019. There were no relieving factors. She had a history of diabetes, poorly controlled hypertension, hyperlipidemia, history of smoking, cardiovascular atherosclerotic disease, prior anteroseptal heart attack, ulcerative colitis, a prior cholecystectomy, prior bowel obstruction surgery, and hysterectomy. She is on mesalamine which weakens her immunity. She was admitted for small bowel obstruction and started on NG tube fluids.
January 14 chest X ray reports left lung collapse (atelectasis), opacity (density/mass) or infiltrate (lung infection).
X ray taken of the abdomen on January 14, showed persistent obstruction and she was scheduled for a diagnostic laparoscopy on January 15.
On January 15, noted in the records that the Patient stated she could not stop shaking, glucose check 243, sbp 130's. patient found to be sensitive to morphine.
EKG revealed a likely prior anteroseptal heart attack. No further evaluation or testing was performed as to her heart and lungs, nor was a cardiologist or pulmonologist consulted.
She was evaluated by the anesthesiologist, who reviewed her medical history and determined to be ASA III and Mallampati II and an appropriate candidate for anesthesia.
The patient was brought to the operating room at 1705. Induction began at 1721. Decedent was intubated at 1723. The tube was secured, and the ventilator was activated with oxygen and air and low dose sevoflurane turned on. At approximately 1731, versed (1 mg), fentanyl (100 mcg), lidocaine (100 mg), propofol (150 mg) and rocuronium (50 mg) were administered while cricoid pressure was held. Dexamethasone (4 mg), metoclopramide (10 mg), and ondansetron (4 mg) were then administered. A few doses of phenylephrine (200 mcg) were administered prior to the incision to maintain resting blood pressure. Two grams of cefazolin were requested by the surgeon and given at 17:43.
The surgeon then made a five-millimeter incision in the right lateral abdomen, a five-millimeter port was then introduced into the abdomen under direct visualization with the help of a five-millimeter laparoscope. The surgeon then attempted to insufflate the peritoneum. However, the pressure was very high, and this was not successful. The surgeon requested a longer five-millimeter port. In the interim, the surgeon decided to insert a Veress needle to insufflate the abdomen. The surgeon made a two-millimeter stab incision in the left upper quadrant two-centimeters below the costal margin at the midclavicular line. The surgeon then inserted a Veress needle into the peritoneum. At that point, the anesthesiologist informed the surgeon that Decedent had a sudden decrease in her end tidal co2, and Decedent was unstable. Shortly thereafter, she became bradycardic. The surgeon withdrew the Veress needle and began chest compressions. At approximately 17:49, the ventilator alarmed to a sudden decrease in end-tidal carbon dioxide on the capnograph. The surgical team was alerted and attempts at insufflation were halted. Within a few seconds, Decedent's heart rate began to decrease. Epinephrine was given to Decedent. Chest compressions were started as the bradycardia had converted into ventricular fibrillation.
Code blue called at 17:50. The anesthesiologist switched the ventilator to manual mode and began to ventilate the decedent by manually squeezing the anesthesia circuit reservoir bag. end-tidal carbon dioxide level remained low. Compressions and ventilation continued with another dose of epinephrine given at approximately 17:55 by another anesthesiologist, who had been called to assist. The anesthesiologist continued to ventilate Decedent throughout the code, and Decedent had bilateral breath sounds as heard with a stethoscope. A second fluid bag was attached to a preexisting IV, and both fluid bags were placed on pressure for volume. Throughout the code, multiple doses of epinephrine, bicarbonate, and calcium were given. Pads were attached early in the code, but no shockable rhythm was ever seen after the initial shock at 17:52. Advanced cardiovascular life support was continued until 18:30 with no improvement in the patient’s condition. Decedent was pronounced dead at 18:30.
Autopsy Report stated:
“Post mortem examination, limited to chest and abdominal cavities, shows marked adhesion related changes involving bilateral lungs, liver, spleen and large and small intestines. No thrombosis or thromboemboli are seen. The left anterior descending exhibit significant calcific stenosis, 30% patent and the .left circumflex artery shows mild stenosis. No acute myocardial infarct is identified. No acute pneumonia or saddle emboli is noted. The liver shows mild steatosis and mild congestion. The kidney demonstrates acute kidney injury. The proximal small bowel shows focal dilation with fecal content. No marked acute inflammatory changes are noted within large and small Intestines.
Overall, the immediate cause of death is unclear. Speculation includes metabolic and hemodynamic instability from underlying small bowel obstruction. The presence of small bowel obstruction and dilation Is most likely secondary to pronounced adhesion, involving multiple organs, including the mesentery and small bowel. There is no histologic evidence of active ulcerative colitis. There is no bowel perforation or bowel injury identified from the latest attempt of laparoscopic procedure.”
Did it fall below the standard of care for the anesthesiologist to determine decedent was an appropriate candidate for anesthesia given her ASA III status due to significant comorbidities including a history positive for 1) smoking 2) diabetes, 3) hypertension, 4) hyperlipidemia, 5) atherosclerotic disease, 6) elderly age > 65 7) prior heart attack, 8) adhesions 9) prior surgeries for bowel obstruction, gallbladder and hysterectomy, 10) an X-ray the morning of the surgery which demonstrated an active lung process occurring in patient and 11) an EKG that same day confirming a likely prior anteroseptal heart attack There had been no cardiac consultation or clearance nor a pulmonary consultation related to her documented heart and lung issues, prior to the procedure.
Did it fall below the standard of care for the anesthesiologist to administer the nature and amount of the anesthesia and other medicines administered to decedent prior to her death?
Did the conduct of the anesthesiologist comply with the standard of care during the code blue?
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Closed Cases
Comments are accepted only from Obstetrics and Gynecology experts.
34 yo female with significant complications following second trimester D&E
Case Overview
Location: FL
34 years old, Female
Past Medical History:
Past Surgical History:
34 yo female with significant complications following second trimester D&E
Date of Procedure: January 22, 2025
Procedure: Patient underwent a second-trimester Dilation and Evacuation (D&E). After Laminaria removal and cervical dilation, a 14mm suction curette and Sopher clamp were used to evacuate the uterine contents. On the final pass, a possible posterior uterine defect was visualized on ultrasound and palpated. Despite unclear confirmation of injury, multiple instrument passes had already occurred.
Due to concern for perforation, diagnostic laparoscopy was initiated and revealed a large expanding hematoma in the right retroperitoneum. Conversion to open laparotomy followed.
Injuries & Surgical Findings: Posterior uterine wall perforation (suspected by ultrasound and instrumentation)
Hemorrhage tracking into the right retroperitoneum, adjacent to the infundibulopelvic (IP) ligament
Ovarian vasculature disruption requiring: Right oophorectomy, Total abdominal hysterectomy, Bilateral salpingectomy, Persistent vaginal cuff bleeding Hematoma involving the right mesentery and cecum (trauma surgery consulted). Activation of massive transfusion protocol, arterial line placed, ICU transfer required
Outcomes
Loss of uterus and right ovary (permanent infertility, premature surgical menopause)
Massive intraoperative hemorrhage
Multidisciplinary intervention required (OB/GYN, Gyn Oncology, Trauma Surgery, Critical Care)
ICU admission post-op
Questions:
Uterine perforation during D&E — instrumentation extended beyond the uterine wall, likely due to Excessive force or depth? Blind use?
Ovarian vasculature injury: well outside normal surgical field?
Delayed recognition of injury — despite signs of perforation on ultrasound, earlier imaging or surgical halt was not performed?
Ultrasound guidance only used after suspected damage; not during curettage or forceps use?
Need for emergency laparotomy and organ removal directly traceable to procedural injury?
Overall concern for intraoperative misjudgment and failure to adhere to procedural safeguards.
Operative notes attached for reference.
Thank you in advance for your time and opinions.
Files:
2 Responses
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
I am a gynecologic oncologist in practice x 10 years at alarge academic center, routinely on back up call for OBGYNs
How often do you encounter cases similar to this one in your practice?
I encounter variations of this scenario - possible perforation, retroperitoneal bleed, intraoperative hemorrhage - on intraoperative consult about once a month or so
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
I have been an obgyn 14 years and done these procedures. Under ultrasound guidance and even with ultrasound it’s challenging. Expanding hematoma would be so very hard to find origin. Also losing one over will not make her menopausal. So at least there is that.
How often do you encounter cases similar to this one in your practice?
I’ve never had one but have heard of a handful over the course of my career
Want to open a case or submit response?
Comments are accepted only from Medical Oncology experts.
Stage IV Diffuse Large B-Cell Lymphoma dx with possible different treatment options
Case Overview
Location: FL
67 years old, Male
Past Medical History:
Cancer
Past Surgical History:
67-year-old male, in early-to-mid 2023 with an enlarging testicular mass in combination with palpable left supraclavicular lymphadenopathy. CT imaging then demonstrated a 2cm RUL pulmonary nodule, a smaller LLL nodule, a destructive left sacral lesion reaching 6cm and a icm peri-pancreatic lymph node. A biopsy of a representative left supraclavicular node diagnosed with Stage IV Diffuse Large B-Cell Lymphoma (DLBCL) on May 4, 2023.
Stage IV with extranodal involvement including:Testes, Skin, Lungs, Retroperitoneum, Multiple lymph node regions (inguinal, iliac, hilar, supraclavicular) IPI Score: High-intermediate (3 points) CD20-positive, meaning responsive to anti-CD20 immunotherapy (like rituximab)
Initial Treatment: IP received 6 cycles of R-CHOP, a standard first-line regimen for DLBCL, completed in September 2023.
He showed excellent response initially with complete metabolic remission on post-treatment PET scan.
Relapse: A PET/CT in December 2023 revealed new metabolically active disease in: Left retroperitoneal nodes, Inguinal nodes, Possibly the left testicle, Biopsy confirmed recurrent DLBCL.
Note from oncology re Treatment Plan Post-Relapse:
“Compelling options for disease which has progressed at such a short interval post-chemotherapy include the cellular therapies: bispecific T-cell engaging agents versus a CAR-T cell based approach. Regarding the autologous CAR-T approach, significant additional time would be needed for line placement, steroid washout followed byT-cell collection, and then finally the CAR-T manufacturing process (if viable), and in his case his disease appears to be progressing relatively rapidly. Either BiTE therapy, which would necessitate frequent visits to and from the clinic for a prolonged duration of treatment/ serial dosing, or allogeneic (i.e. "off-the-shelf") CAR-T stand out as acceptable and appealing options. The pros and cons of each approach were discussed with the patient, who favors being screened for our caribou (ANTLER) trial -- which may hopefully culminate in him receiving an allogeneic CAR-T product at a shorter duration than would be the case with autologous CAR-T. In this case, any native T-cell compromise from prior chemotherapy and/ or recent prolonged steroid therapy would not be an issue.”
Bone marrow biopsy in April 2024.
Prior to any further treatment, died in May 2024.
Genetic Testing in This Case Attached.
The family was told that other options and/or bone marrow biopsy was possibly indicated earlier for possible different outcome.
Thank you in advance for any opinion on this.
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2 Responses
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
I have testified on the defense side in 8 cases and done 5 depositions.
How often do you encounter cases similar to this one in your practice?
this is a rare case. I have treated testicular DLBCL.
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
I am board certified hematologist and oncologist practicing over 10’years and have managed severe cases of DLBCL. I also get referrals from other oncologists for complex DLBCL for patients to guide management.
How often do you encounter cases similar to this one in your practice?
I see about 20-50 new cases annually
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Comments are accepted only from Neurological Surgery experts.
Delay in diagnosis of anterior communicating aneurysm with intracerebral hemorrhage.
Case Overview
Location: FL
62 years old, Female
Past Medical History:
HTN
Past Surgical History:
neck fusions
The case involves a delay in diagnosis of anterior communicating aneurysm with intracrebral hemorrhage.
The patient was a 62 year old female who was taken by EMS from her home to a community hospital for headache of one hour and neck pain. She had a known history of hypertension and was a smoker. The emergency department providers did not document complaints of headache that were noted by EMS and instead worked up the patient's neck pain. Patient's glasgow coma scale was 15.
The patient arrived to the emergency department at 8:14 pm. At 2:44 am, a CT of the head, without contrast, was performed due to altered mental status that showed 6.8 x 3.5 cm left frontal/temporal acute subcortical intraparenchymal hematoma, 3.2 x2. 7 cm left anterior frontal acute subcortical hematoma, and 5.4 x 1.6 cm acute cavum septum intra ventricular hematoma as well as a 7.2 mm midline shift. The patient's glasgow coma was 10 and then later noted to be 8.
A CTA was ordered to rule out an aneurysm. The radiolgist identified an acute intraparenchymal hemorrhage in the left temporal lobe and left frontal lobe region with intraventricular blood in the third ventricle. subarachnoid blood products are also
seen in the suprasellar cistern, the right temporal lobe and the left temporal lobe region. This results in mild rightward midline shift with early subfalcine herniation and mild effacement of the fourth ventricle.
However, the radiologist failed to see an aneurysm.
As a result, the patient was sent to another facility that did not have vascular neurosurgical services. At this facility, the on-call neurosurgeon reviewed the CTA and identified an aneurysm on imaging. For this reason, the patient was then sent by helicopter to another facility with appropriate neurosurgical services. Her glascow coma scale was 3.
At 15:00, the patient underwent a left craniotomy and complex anterior communicating artery aneurysm clipping with left temporal ICH evacuation. The surgery occurred 19 hours after the patient arrived at the first hospital. The pre-operative CTA identified a 2 mm saccular aneurysm at the right carotid terminus near the origin of the PCOM with an inferiorly projecting 7 mm saccular aneurysm that appears to originate from the anterior communicating artery on the right. Probable 2 mm saccular aneurysm
extending from the left A-comm.
The question is whether earlier surgical intervention would have made a difference in a patient who now suffers memory loss, difficulty walking, incontinence due to forgetfulness, and lives in a memory unit of an assisted living facility.
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2 Responses
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
I am a board-certified neurosurgeon with fellowship training in cerebrovascular surgery (aneurysm clipping) and current experience taking call in stroke and trauma centers where these cases are commonly encountered. I have reasonable experience in depositions and court proceedings, and ability to communicate medical information to lay audiences in a clear manner.
How often do you encounter cases similar to this one in your practice?
I encounter roughly 10 cases per year which are ruptured aneurysms with ICH. The incidence of aneurysmal SAH in the general U.S. population is about 6–10 cases per 100,000 people per year. Therefore even busy ERs have low numbers, but the patterns and treatment protocols are well established.
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
My significant expertise in brain aneurysm treatment
How often do you encounter cases similar to this one in your practice?
Every week and sometimes multiple times a week
Want to open a case or submit response?
Comments are accepted only from Internal Medicine - includes all subspecialties experts.
Post cervical laminectomy, possible delayed diagnosis of CSF infection
Case Overview
Location: FL
68 years old, Male
Past Medical History:
HTN, COPD
Past Surgical History:
laminectomy
68 year old with cervical myelopathy and cervical stenosis. He is a heavy smoker and not a candidate for fusion. Has c4-5, c5-c6 cervical laminectomy on Jun 10, 2024
OP note unremarkable, D/C 2 days later ambulating and voiding, PO intake and Hemovac.
June 13, 2024 returns to ER for pain control and increased shortness of breath. He is admitted for COPD exacerbation, consult to neuro for post-op eval. Did not require O2 at home, however now requires 2 lpm to maintain O2 sat above 95%.
Neurology defers mostly to IM for COPD maintenance, noting no specific neurological symptoms associated with surgery.
Radiology done includes CXR, Head CT and CTA chest. Unremarkable. Despite being afebrile throughout, WBC on admit is 10.0. It rises to 12.1 on day 2 then 16.1 on discharge. There is no specific mention of the rise in WBCs during admission and notes of not likely infectious process? Blood pressures are soft in the 100s, but no tachycardia. JP drain placed post-op is showing serosanguineous output 100-150mls per day during admission, however no cultures drawn on fluid. No blood cultures. No further radiology on neck/spine. This is all chalked up to balancing opioids/COPD.
D/C on June 19, 2024 with home oxygen and Augmentin 7 day PO.
Returns the next day, June 20 for increased pain and hypoxia. Gave gabapentin, muscle relaxants, and multimodal pain control with good effect No breathing issues during pain management. Physical Therapy (PT) recommended inpatient rehab due to residual pains and need for functional therapy. Neurosurgery recommended keeping spinal drain in place due to high output, but still no exploration of CSF leak during the first 3 days. Initially planned for rehab on 6/24, but that night, spiked a fever (101°F), became extremely drowsy, altered mental status. Vitals normal, no hypercapnia, clinically dry, so given IV fluids. Blood, urine, and spinal drain cultures obtained.
Started on Levaquin (quinolone antibiotic) due to severe penicillin/cephalosporin allergies. Suspected UTI initially (mucus plug noted on catheterization). Later, spinal drain culture grew Gram-negative rods, so Infectious Disease (ID) consulted.
CSF (spinal fluid) cultures grew multiple bacteria & fungi: Serratia marcescens, Acinetobacter, Candida dubliniensis, Granulicatella adjacens, Enterococcus faecalis. CSF lab values: WBC3,467 CSF glucose: 16 CSF protein: 167 Concern for associated osteomyelitis (bone infection). Hemovac drain removed by Neurosurgery on 07/01/2024.
Physical therapy recommended inpatient rehab. Neurology & Infectious Disease recommended outpatient follow-up. Discharged finally on 7/8/2024
Antibiotic Treatment Plan: IV vancomycin and meropenem started, fluconazole added by ID. Prolonged IV antibiotics required for 6 weeks. Meropenem (1g IV every 8 hours) and Fluconazole (400mg PO daily) to continue until 8/16/2024.
Was there a failure to timely diagnose the CSF infection during the June 13 admission? Possible hospital-acquired infection due to poor infection control? Delay in appropriate antibiotic treatment?
Thank you in advance
Files:
7 Responses
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
Having managed many cases with severe infections in the inpatient and outpatient setting since I work at a center which has robust spine surgery program.
How often do you encounter cases similar to this one in your practice?
It is variable but generally around 6-10 cases annually. We have a low threshold to scan and identify source of infection.
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
I see hundreds of these cases during my career as ID specialist. In addition, the bacteria and candida that grew from the JP drain seems to be gut flora and likely the patients had poor compliance in keeping the JP drain in a clean environment
How often do you encounter cases similar to this one in your practice?
I see these cases All the time The major problem on this back surgeries is that the back gets contaminated easily due to patients position in bed or contamination due to poor maintaince of JP drain
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
I have been reviewing medical malpractice cases since 2012. Between 60-80 cases in total. I am well aware of cases in which inappropriate evaluation of infection leads to systemic infection and further morbidity and mortality.
How often do you encounter cases similar to this one in your practice?
I do see occasional cases that are admitted to the inpatient service.
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
Neurocritical care, over 20 years of experience managing post-op neurosurgical complications
How often do you encounter cases similar to this one in your practice?
Infrequently, since these are rare complications, we see a bunch of sepsis post-op and CSF leaks.
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
Ideal expert is ID which I am not
How often do you encounter cases similar to this one in your practice?
Very unsual to have GNR infection from the surgery
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
I’ve seen patients in the hospital with similar postop complications and infections that have emerge. I’ve also seen them in my outpatient practice and follow up. Were we immediately sent the patient to the ER for evaluation of CSF and other causes for infection and imaging.
How often do you encounter cases similar to this one in your practice?
Encounter cases in which I have to do hospital follow up weekly. I have encountered cases just like this with complications from a procedure that may be infection or other impacts on kidney and organ function once every 3 to 6 months
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
This is a multidisciplinary case involving not only neurosurgery, but also internal medicine (I completed my IM training at Johns Hopkins in 2010), infectious disease, and so forth. I myself have had a CSF leak and can thus picture/understand what this patient went through consequent to delayed diagnosis, which I also myself went through.
How often do you encounter cases similar to this one in your practice?
I would say on a near weekly basis I encounter cases of cryptogenic infection/leukocytosis. Various specialties and sub-specialties have to come together to find the source and come up with a treatment plan once that’s been achieved (or empiric therapy if a clear source can’t be found).
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Comments are accepted only from Pediatrics - Cardiology experts.
Newborn with AVCD repair has multiple post-op complications, dies at 15 months old.
Case Overview
Location: FL
2 years old, Male
Past Medical History:
As mentioned in the narrative
Past Surgical History:
The decedent is a 15-month-old male born at 37 weeks and 3 days with congenital heart disease, polydactyly of left foot (status post removal of postaxial toe), failed hearing test, abnormal involuntary movements, central hypotonia, gross motor defects, bilateral undescended testes, and phimosis. Pregnancy was complicated by polyhydramnios, gestational hypertension, and intrauterine growth restriction. Genetic analysis identified him as having SETD5-related neurodevelopmental disorder. Was dx with AVCD prenatally and confirmed after birth.
He followed with pediatric cardiology in an outpatient setting, and echocardiogram studies showed a transitional atrioventricular canal defect, large primum and small secundum atrial septal defects, right atrium dilation, mild right atrioventricular valve insufficiency, and mild left atrioventricular valve regurgitation due to a cleft directed to the right atrium. Due to worsening right heart dilation and left to right shunting, he underwent surgery for repair of the transitional atrioventricular canal defect, left atrioventricular valve cleft closure, and patch closure of atrial septal defect. Post-repair transesophageal echocardiogram was reassuring and he was extubated. Overnight he developed lactic acidosis with hypotension and repeat echocardiogram showed new severely depressed biventricular function with evidence of pulmonary hypertension.
He additionally developed clinlcal signs of infection, and was placed on VA-ECMO three days following his operation in order to recover lung and cardiac function.
His ventricular and pulmonary function improved, and he was decannulated from ECMO approximately five days following. However, shortly after this he developed intermittent fevers, elevated C-reactive protein, elevated white blood cell count, and acute desaturation requiring intubation. Chest x-ray showed a completely consolidated right lung. Bronchoscopy was attempted to inflate the right lung but was unsuccessful and distal tracheomalacia and mild right bronchomalacia were noted. His blood cultures showed no growth, and respiratory viral panel was negative. He was given broad-spectrum empiric antibiotics. He developed acute hypercarbic respiratory failure; chest x-ray showed pulmonary edema. He underwent cardiac catheterization, which showed restrictive pathology, although coronaries were unremarkable.
Approximately two weeks following his procedure, he was transferred to different pediatric specialty facility for further management and heart transplant evaluation. Karius testing identified Achromobacter xylosoxidans and he was treated with multiple antibiotics. He had abrupt significant worsening of pulmonary edema, with only transient improvement with increased diuresis. Subsequently, he acutely desaturated, became bradycardic, and developed pulseless electrical activity. Acute cardiovascular life support was conducted with return of spontaneous circulation after 23 minutes.
Despite maximal vasopressor support, he developed multiorgan system failure. The decedent passed shortly after switching to comfort care.
Significant findings at autopsy included an enlarged heart with evidence of prior procedure with an intact patch and evidence of healing on histology. The pericardium was roughened, and fibrin deposition without significant inflammation was identified on the pericardium and epicardial surfaces. Bilateral lungs showed evidence of diffuse alveolar damage and parenchymal hemorrhage. The liver showed diffuse near bridging centrilobular necrosis, and the kidneys showed evidence of acute kidney injury. The brain showed hypoxic injury.
Looking for a pediatric cardiologist familiar with this condition to determine if the course of events and treatment plan was reasonable/within SOC or if there were possible opportunities for deviations.
Attached you will find updated progress notes from the last facility the IP was admitted to for reference.
Please notify of any questions. Thank you in advance.
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2 Responses
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
More than 25 years in pediatric cardiology in academic and private setting. I primarily work in pediatric echocardiography and TEE.
How often do you encounter cases similar to this one in your practice?
We have an active full service CVICU with many similar pts.
Do you believe there might have been medical error?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
What makes you a good expert for this case?
I have been practicing pediatric cardiology and managing patients pre and post operatively for 35 years at a children's hospital with a moderate size pediatric cardiology and peds cardiothoracic surgical program. I have seen many cases of children with primum ASD's undergo this type of surgery
How often do you encounter cases similar to this one in your practice?
This would be considered an unusual postoperative course for a child with an isolated primum ASD and cleft mitral valve who is otherwise asymptomatic
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