Background

Enteral antibiotics are rarely used in intensive care units. IV access can be problematic in children with prolonged hospitalizations. We wanted to report our enteral antibiotic use in PICU.

Objectives

....................................

Methods

Retrospective descriptive study performed in a tertiary PICU

Results

30 patients (53% female) received enteral antibiotics between 2016-2018. Median age was 18 months (IQR 6-35). Median PRISM mortality rate was 5.3 (IQR 3.9-17). Majority (80%) were intubated, and 2% received inotropic support. Patients had mostly neurologic diseases (73%) and malignancies (16%) Median WBC, platelets and CRP were 14.4x10³/mL (IQR 10.5- 18), 235000 (IQR 102000-412000) and 42.5 (IQR 16-91.5) respectively.

Types of pathogens and antibiotics are presented in Table and Figure.

Nine patients (30%) had ventilator associated pneumonia (VAP), 14 (46%) urinary tract infections (UTI), 6 (20%) blood stream infections (BSI) (1 associated with mediastinitis) and 1(0.03%) ventriculitis. Four patients were switched to enteral antibiotics after antibiogram was obtained. Mediastinitis/BSI case was switched to enteral after 1 week of parenteral treatment. All patients were treated successfully.

Conclusion

When IV access is limited and enteral absorption is not problematic, enteral antibiotic use can be a safe alternative for treatment of appropriate infections.

Background

Nosocomial infections are frequently seen in hospitalized patients due to traumatic brain injury.

Objectives

The incidence of infection in traumatic brain injury(TBI), its relationship with risk factors, hospital cost and duration of hospital stay.

Methods

63 patients were hospitalized in the pediatric intensive care unit of Marmara University Hospital between 2012 and 2014 for the treatment of severe TBI.

Results

There were no significant differences in terms of age, sex, length of stay, type of ventilation, presence of central catheter and duration of antibiotic treatment and infection development in patients with and without infection. Foley catheter and nasogastric catheter uses were more common in trauma patients. 5 patients were developed infection and the ratio is 7,9% . 3 of the infections developed in trauma patients were ventilator related pneumonia, 1 was urinary tract and 1 was catheter related infection.

Conclusion

There are risk factors that may cause nosocomial infection in patients with severeTBI(1). These infections increase the duration of hospital stay and the cost of treatment. The nosocomial infection ratio was % 3-14(1,2) and our rate was % 7,9. In a study by Zolldan et al. In 763 patients between 1998-2002; urinary tract infection rate was 24.7%, pneumonia 23.6% and bacteremia 17.2% (2). Prospective studies are needed to evaluate more patients in our country.

References:

1- Alharfi I.M et all. Infection rates, fevers and associated factors in pediatric severe traumatic brain injury. Journal of Neurotrauma . 2014:31;452-458.

2-Zolldan D, Thiex R,et all. Periodic surveillance of nosocomial infections in a neurosurgery intensive care unit. İnfection 2005;33:115-21.

Background

Hyperchloremia can be caused by renal failure, renal tubular acidosis, dehydration, diabetes insipidus, gastrointestinal bicarbonate loss, excessive fluid replacement therapy with sodium chloride, as well as diuretics, corticosteroids and acetazolamide use. Here we present a fatal hyperchloremia case which was associated with Munchausen by proxy syndrome.

Objectives

An 8 month old male was admitted to our PICU due to decompansated shock after an episode of gastrointestinal bleeding. Past medical history was significant for multiple hospitalizations due to recurrent fevers, various rashes, respiratory distress, vomiting. His metabolic and immune panels were normal.

On PICU admission his blood pH was 6.93, PC02:42mmhg, HCO3: 8.3mmol/L, BE: -23.6mmol/L, lactate :2.9mmol/L, Na:133mmol/L, Cl: 363mmol/L (N:98-106) and methemoglobin was 21.2% (N:0-1.5). The twıce normal range of hyperchloremia with mild hyponatremia could not be attributed to an intrinsic medical problem. He had burn like oral lesions, and developed esophageal perforation presenting with pneumomediastinum and pneumothorax. The child expired due to multisystem organ failure. The autopsy results were consistent with enteral intake of HCL. Further history revealed that the child had been referred to Child Protection Services due to a suspicious history and symptoms during his previous hospitalizations.

Methods

..................................

Results

........................................

Conclusion

Excessive chloride intake should be kept in mind when a patient’s chloride levels are so high that cannot be related to any disease. Munchausen by proxy syndrome should be remembered when a patient presents with rare and extraordinary symptoms, and does not respond to the standard therapy as in our case.

Background

Pneumococcal meningitis is well known to cause vasculopathy and ischemic infarcts. Here, we present an unvaccinated case of pneumococcal meningitis with complicated fatal course.

Objectives

A 12 year old male presented to the ER with fever, headache, lethargy and difficulty in balance. His PMH was significant for recent left myringotomy and tube placement three weeks earlier, due to hearing loss with past ear infections. His work up revealed pneumococcal meningitis, for which ceftriaxone and vancomycine was initiated promptly. Initial tomogragraphy was normal except decreased aeration of mastoid cells. Due to anaphylaxis with ceftriaxone, patient developed severe upper respiratory obstruction, he was intubated, given epinephrine and switched to meropenem with concurrent application of steroids. Repeat CT due to anisocoria revealed infarcts in medulla oblongata and on both cerebellar hemispheres, along with left mastoid abscess. A colesteatoma is detected on mastoidectomy operation which was resected. Anisocoria regressed and patient became responsive to verbal stimuli. Osmolar therapy was given for brain edema. However, anisocoria recurred and re-imaging revealed hydrocephalus, necessitating emergent EVD and subsequent craniectomy due to impending tonsillar herniation. The patient died on the 12^thday of PICU admission. His CSF was clear of infection and no immune deficiency could be found.

Methods

........................

Results

...................................

Conclusion

Despite appropriate interventions, pneumococcal meningitis can lead to vasculitis, causing infarcts and hemorrhage. Vaccination is important key for prevention of fatal meningitis.

Background

Asparagine synthetase(ASNS) deficiency is a neurometabolic disorder first described in 2013. There are 21 cases known until now. Here we present an ASNS deficiency case who presented with microcephaly and apneic seizure and whose cranial screening was normal at admission. However, massive ventriculomegaly and brain atropy developed in just one month.

Objectives

A microcephalic 40 days old female born to consanguinous parents presented with apnea and seizure. She was intubated and admitted to our PICU. On examination, her anterior fontanel was closed, deep tendon reflexes were brisk and she had clonus. Hyperexplexia was also detected and there was no spinal defect. CBC and biochemical markers were within normal range. Cranial CT showed neither structural anomaly nor hemorrhage (fig1). CSF examination was not compatible with infection. Toxoplasmosis, rubella, cytomegalovirus, herpes simplex virus serologies were negative. Metabolic screening was negative. The patient had a prominent clonus, and did not have any active seizure. Due to inability to extubate cranial screening was repeated. Here was a major cerebral and cerebellar atrophy and massive ventriculomegaly. Pons was atrophic as well. (fig2). A homozygous c.1394G>A p. (Arg 465G1n) mutation was detected on ASNS gene, as a result of whole exon analysis.

Methods

.......................

Results

........................

Conclusion

ASNS exists in many cells', tissues' and organs' structure however, it shows as neurological impairment when it malfunctions. It is characterised by congenital microcephaly, progressive brain atrophy,severe neurodevelopmental delay,persistent seizures. Other features include axial hypotonia, appendicular hypertonia, hyperreflexia. Cranial MRI findings include thin cerebral cortex, cerebral volume loss, flattening of the gyri, volume loss in the pons.

Background

Galen vein aneurysm can present with hydrocephalus. Here we present a complicated case necessitating multiple EVD placements after the embolization procedure.

Objectives

An 8 month old patient with history of ventriculoperitoneal (VP) shunt operation for hydrocephalus (Fig1) presented with a seizure and magnetic resonance imaging revealed 3 giant and 50 smaller size aneurysms and an arteriovenous malformation (Fig 2). Interventional radiology proceeded with an embolisation procedure for his arteriovenous fistula and he was admitted to our PICU. His VP shunt was externalized due to intraventricular bleeding after this procedure (Fig 3) His EVD was changed 15 times at the bedside due to clogging with bloody debris within 3 months’ period. All CSF screening cultures remained sterile and his shunt was internalized with clearance of blood in CSF. Unfortunately this lasted only a week, and his shunt was externalized again due to a dysfunction. Thereafter he developed ventriculitis caused by methicillin sensitive staphylococcus aureus and his EVD was changed for 7 more times. Bilateral interventions were performed aiming more effective CSF drainage without success. The child expired on 7 months after his admission due to progressive neurologic dysfunction.

Methods

.............................................

Results

Intraventricular hemorrhage after an embolization procedure may require many interventions for drainage of CSF. 23 EVD placements were performed, which was the highest number for a single patient in our unit.

Conclusion

.....................................

Background

Vomiting, poor weight gain and respiratory problems are generally attributed to gastrointestinal reflux disease in infants. Here, we present a case who underwent further examination because of vomiting, failure to thrive and respiratory distress.

Objectives

A 3 month old male as transferred to our pediatric intensive care unit (PICU) due a seizure followed by cardiorespiratory arrest while being hospitalized due to gastrointestinal reflux disease and respiratory distress attributed to pneumonia. His symptoms were of 6 weeks duration, for which he was admitted twice for work up and therapy. Trial of antireflux treatment was not successful. His further workup included bronchoscopy to rule out laryngomalacia and reflux and an esophago-gastro-duodenal screening . Despite preemptive antibiotic treatment and antireflux medications symptoms did not regress Following a generalized seizure, he arrested on the ward. Cranial tomography showed hydrocephalus due to a posterior fossa tumor. After intubation and supportive management, he was transferred to our PICU for surgical management. He underwent an emergent ventriculoperitoneal shunt, followed by subtotal resection of the massive tumor. Pathology showed atypic rhabdoid teratoid tumor.

Methods

................................

Results

..........................

Conclusion

Central nervous system tumors are the most common solid tumors seen in childhood and children may present with reflux symptoms. This should be kept in mind when infants have persistent symptoms despite antireflux therapy.

Background

Enteral antibiotics are rarely used in intensive care units. IV access can be problematic in children with prolonged hospitalizations. We wanted to report our enteral antibiotic use in PICU.

Objectives

....................................

Methods

Retrospective descriptive study performed in a tertiary PICU

Results

30 patients (53% female) received enteral antibiotics between 2016-2018. Median age was 18 months (IQR 6-35). Median PRISM mortality rate was 5.3 (IQR 3.9-17). Majority (80%) were intubated, and 2% received inotropic support. Patients had mostly neurologic diseases (73%) and malignancies (16%) Median WBC, platelets and CRP were 14.4x10³/mL (IQR 10.5- 18), 235000 (IQR 102000-412000) and 42.5 (IQR 16-91.5) respectively.

Types of pathogens and antibiotics are presented in Table and Figure.

Nine patients (30%) had ventilator associated pneumonia (VAP), 14 (46%) urinary tract infections (UTI), 6 (20%) blood stream infections (BSI) (1 associated with mediastinitis) and 1(0.03%) ventriculitis. Four patients were switched to enteral antibiotics after antibiogram was obtained. Mediastinitis/BSI case was switched to enteral after 1 week of parenteral treatment. All patients were treated successfully.

Conclusion

When IV access is limited and enteral absorption is not problematic, enteral antibiotic use can be a safe alternative for treatment of appropriate infections.

Background

Nosocomial infections are frequently seen in hospitalized patients due to traumatic brain injury.

Objectives

The incidence of infection in traumatic brain injury(TBI), its relationship with risk factors, hospital cost and duration of hospital stay.

Methods

63 patients were hospitalized in the pediatric intensive care unit of Marmara University Hospital between 2012 and 2014 for the treatment of severe TBI.

Results

There were no significant differences in terms of age, sex, length of stay, type of ventilation, presence of central catheter and duration of antibiotic treatment and infection development in patients with and without infection. Foley catheter and nasogastric catheter uses were more common in trauma patients. 5 patients were developed infection and the ratio is 7,9% . 3 of the infections developed in trauma patients were ventilator related pneumonia, 1 was urinary tract and 1 was catheter related infection.

Conclusion

There are risk factors that may cause nosocomial infection in patients with severeTBI(1). These infections increase the duration of hospital stay and the cost of treatment. The nosocomial infection ratio was % 3-14(1,2) and our rate was % 7,9. In a study by Zolldan et al. In 763 patients between 1998-2002; urinary tract infection rate was 24.7%, pneumonia 23.6% and bacteremia 17.2% (2). Prospective studies are needed to evaluate more patients in our country.

References:

1- Alharfi I.M et all. Infection rates, fevers and associated factors in pediatric severe traumatic brain injury. Journal of Neurotrauma . 2014:31;452-458.

2-Zolldan D, Thiex R,et all. Periodic surveillance of nosocomial infections in a neurosurgery intensive care unit. İnfection 2005;33:115-21.

Background

Hyperchloremia can be caused by renal failure, renal tubular acidosis, dehydration, diabetes insipidus, gastrointestinal bicarbonate loss, excessive fluid replacement therapy with sodium chloride, as well as diuretics, corticosteroids and acetazolamide use. Here we present a fatal hyperchloremia case which was associated with Munchausen by proxy syndrome.

Objectives

An 8 month old male was admitted to our PICU due to decompansated shock after an episode of gastrointestinal bleeding. Past medical history was significant for multiple hospitalizations due to recurrent fevers, various rashes, respiratory distress, vomiting. His metabolic and immune panels were normal.

On PICU admission his blood pH was 6.93, PC02:42mmhg, HCO3: 8.3mmol/L, BE: -23.6mmol/L, lactate :2.9mmol/L, Na:133mmol/L, Cl: 363mmol/L (N:98-106) and methemoglobin was 21.2% (N:0-1.5). The twıce normal range of hyperchloremia with mild hyponatremia could not be attributed to an intrinsic medical problem. He had burn like oral lesions, and developed esophageal perforation presenting with pneumomediastinum and pneumothorax. The child expired due to multisystem organ failure. The autopsy results were consistent with enteral intake of HCL. Further history revealed that the child had been referred to Child Protection Services due to a suspicious history and symptoms during his previous hospitalizations.

Methods

..................................

Results

........................................

Conclusion

Excessive chloride intake should be kept in mind when a patient’s chloride levels are so high that cannot be related to any disease. Munchausen by proxy syndrome should be remembered when a patient presents with rare and extraordinary symptoms, and does not respond to the standard therapy as in our case.

Background

Asparagine synthetase(ASNS) deficiency is a neurometabolic disorder first described in 2013. There are 21 cases known until now. Here we present an ASNS deficiency case who presented with microcephaly and apneic seizure and whose cranial screening was normal at admission. However, massive ventriculomegaly and brain atropy developed in just one month.

Objectives

A microcephalic 40 days old female born to consanguinous parents presented with apnea and seizure. She was intubated and admitted to our PICU. On examination, her anterior fontanel was closed, deep tendon reflexes were brisk and she had clonus. Hyperexplexia was also detected and there was no spinal defect. CBC and biochemical markers were within normal range. Cranial CT showed neither structural anomaly nor hemorrhage (fig1). CSF examination was not compatible with infection. Toxoplasmosis, rubella, cytomegalovirus, herpes simplex virus serologies were negative. Metabolic screening was negative. The patient had a prominent clonus, and did not have any active seizure. Due to inability to extubate cranial screening was repeated. Here was a major cerebral and cerebellar atrophy and massive ventriculomegaly. Pons was atrophic as well. (fig2). A homozygous c.1394G>A p. (Arg 465G1n) mutation was detected on ASNS gene, as a result of whole exon analysis.

Methods

.......................

Results

........................

Conclusion

ASNS exists in many cells', tissues' and organs' structure however, it shows as neurological impairment when it malfunctions. It is characterised by congenital microcephaly, progressive brain atrophy,severe neurodevelopmental delay,persistent seizures. Other features include axial hypotonia, appendicular hypertonia, hyperreflexia. Cranial MRI findings include thin cerebral cortex, cerebral volume loss, flattening of the gyri, volume loss in the pons.