Principles of Acute Pediatrics

Principles of Acute Pediatrics

Part A: Concept map for the effects of Dilated cardiomyopathy (DCM)

Not able to keep up with others

Unable to play

Restriction to family outings

Medical Alert Bracelet required

Often special Diet is required

Frequent checkups

Health

Tutor requirement

High Absenteeism

Poor Esteem

Fear of Death

Play

Learning

School

Grief

Resentment

Parents

Resentment

Child

More attention to the sick

Sibling Rivalry

Family Dynamics

Psychology

Effects of DCM on children and their families

 

 

 

 

Part B: Epilepsy/seizures

Introduction and case stating

Epilepsy refers to a complex brain disorder that is marked by prolonged, disorderly and recurrent nerve tissue discharge that results in convulsions (NSW Department of Health, 2009, p. 5). It may involve various pathological conditions of the brain.  Seizures are mild clinical manifestations of abnormal and excessive neuronal discharge that is due to an underlying disease. In rare cases, seizures result in epilepsy development. According to Lee et al. (2011, p. 279), seizures often occurs for less than 7 minutes while SE exists for about 30 minutes.

This section seeks to explore seizures in children using a case study of a five-year-old male patient. The patient had been well for the first two years after which he started to experience quick jerks that deteriorated to successive seizures lasting for about 20 minutes. The patient had been diagnosed with flu prior to the onset of seizures. The family had no history of neurological disorders. However, one of the relatives, a cousin, had also experienced similar seizure attacks after being diagnosed with flu.

Signs and symptoms

The clinical signs and symptoms of seizures vary distinctively. These variations depend on the type, the area of onset, brain maturity of the child, medications if any and the pattern of its propagation (Fisher et al., 2005, p. 1). In this case, the child experienced prolonged seizures lasting for more than 20 minutes. Moreover, the developmental history and the neurological condition were in good condition. The child experienced generalised tonic-clonic seizures. Moreover, the seizures occurred severally in a span of 24 hours and would occur in close succession.

Diagnosis

Diagnosis is primarily through the examination of the medical history of the child and the family. The physician should seek to determine the cause of the fever, febrile seizures history of the family, any prior medication that could have been used and immunisation history (Karande, 2007, p. 1). Infection with meningitis should be eliminated to avoid misdiagnosis (Tatum, Sirven & Cascino, 2014, p. 15). Neurological examination was done using an electroencephalogram [EEG]. The EEG revealed that the neurological condition of the patient was good. However, the child does not have an abnormal developmental history and hence there was no need for performing neuroimaging. Therefore, neuroimaging is not necessary (Jan, 2012, p. 74).

Headinjury during early childhood, metabolic derangement and high fever can cause seizures (NSW Department of Health, 2009, p. 5). Fever can cause seizures in various ways. According to Dubé et al. (2007, p. 1), one such way involves susceptibility to febrile seizures due to genetic conditions. This genetic linkage is due to the interaction of the gene and the environment. Moreover, the mediators of fever result to the generation of febrile seizures. Such mediators include cytokines and other inflammatory biochemicals that are capable of enhancing the excitability of neurons. Moreover, fever can induce alkalosis of the neuronal environment. Such occurrence results in further enhancement of the excitability of neurons.

Treatment

Treatment can be used to eliminate or to reduce seizures. Treatment can involve medication, vagal nerve stimulation, surgery or through ketogenic diet. Treatment depends on type of seizures. Determination of the seizure type enables choosing of the most appropriate drug with antiepileptic drugs being commonly used. However, there has been concern over side effects and response to epileptic medications. Moreover, Lee et al. (2011, p. 280) argues that the administration route and dose for children are problematic for many clinicians.

As earlier stated, the patient is suffering from complex seizures. Therefore, it would be prudent to use an active method of treatment (Jan, 2012, p. 74). Such method of treatment would enable assessment of the respiratory and circulatory status.  A first choice drug should then administered intravenously. For instance 0.4 mg/kg diazepam can be used. Seizures should then be monitored to determine if they persist. Active treatment would be essential in this case due to the side effects of diazepam that causes respiratory suppression (NSW Department of Health, 2009, p. 13). In cases when the seizures are persistent, intermittent treatment with diazepam may be used. Sadleir and  Scheffer (2007, p. 1) argue that it is prudent to use diazepam since it has been shown to reduce chances of febrile recurrence in the case of fever.

In other cases, the antiepileptic drugs (AED) used for the treatment of seizures vary significantly depending on such as effectiveness, route of administration, application, dosage and also the type of epilepsy being treated. Upon determination of the type of epilepsy, monotherapy should be initiated with a drug of first choice (Browne & Holmes, 2008, p. 151). Examples of first choice drugs include diazepam, midazolam, carbamazepine, phenytoin, and oxcarbazepine (Brown & Holmes, 2008, p. 152; NSW Department of Health, 2009, p. 13).

Monotherapy is preffered in seizure treatment. Failure of monotherapy requires administration of a second synergistic AED. The second AED should not contribute to first drug side effects but should help in alleviating seizure effects (NSW Department of Health, 2009, p. 12). Moreover, it should have high solubility to appear in cerebrospinal fluid. According to NSW Department of Health (2009, p. 14), drugs for refractory epileptics involve phenobarbitone, valproate, fosphenytoin and phenytoin.

Some patients may be more response to surgical treatment rather than medication (Browne & Holmes, 2008, p. 162). This mode of treatment is dependent on indications and the contraindications for surgery in epilepsies. Contraindications such benign epileptic conditions may utilise surgery. On the other hand, surgery cannot be used for the treatment of contraindications such as psychosis and family dysfunctional.

Role of a nurse in care for the child and his family

Various effects such as anxiety, fear and social stigmatisation mark the onset of epilepsy. Therefore, the role of nurses in supporting epileptic children and their families has a broad scope. Kelo, Martikainen and Eriksson (2013, p. 71) argue that the broad scope is because of the care required for children and psychological support to the parents. In this case, the nurse is required to provide information regarding the state of the child to the parents. Such information may involve assurance to the parents that the condition is manageable. Moreover, the nurse should eliminate any worries of the parents if present of their child having mental condition, which is usually the case in similar cases. The nurse can play a crucial role in counselling the child who may be experiencing social stigmatisation due to his condition (Kelo, Martikainen & Eriksson, 2013, p. 72). According to Smith and Martin (2008), it would be prudent for the nurse to keep the records of the recovery of the child and refer them for specialised care in case of future complications.

 

 

 

 

 

138 Assessment 3b, Question 2: Diabetic      Ketoacidosis (DKA)

DKA is associated with cases of cerebral oedema. Cerebral oedema occurs in children within 6-12 hours during treatment of DKA. The type and regime of treatment of DKA influence the occurrence of cerebral oedema.

Children with DKA often suffer from dehydration and electrolyte loss. The initial 24 hours of fluid replacement are, therefore, crucial in DKA management. Such fluid replacement is also necessitated by other factors that include vomiting, nausea and diarrhea (Craig et al., 2011, p. 12). Initial fluid replacement should incorporate 0.9% sodium and potassium chlorides.  However, potassium chloride should not be included in case the patient suffers from renal failure. The fluid and the biochemicals should be corrected slowly. Moreover, the sodium level should also be ensured that it does not fall while glucose concentration falls. Slow fluid correction and ensuring that sodium levels rise while glucose level falls helps to avoid development of cerebral oedema complication (The Royal Childrens Hospital Melbourne, 2015, p. 1). The fluid should be administered intravenously. IV fluid administration is crucial for the restoration of peripheral circulation. Hyperventilation prevents changes in cerebral blood flow. If changes in the blood flow occur, it influences the development of cerebral oedema (The Childrens Hospital at Westmead, 2013, p. 15).

The serum potassium is normal in children with DKA while that of the body is depleted. Vanelli and Chiarelli (2003, p. 65) claims that acidosis and hyperglycemia cause potassium to move from the intracellular to the extracellular compartment. Moreover, the potassium level in the body and that of the serum vary due to the symptoms associated with DKA. DKA results in various causal symptoms such as hypertonicity, proteolysis and glycogenolysis. Hypertonicity, proteolysis and glycogenolysis cause loss of potassium from the intercellular compartment into the extracellular fluid (Wolfsdorf et al., 2007, p. 36). Once potassium is in the extracellular fluid, it is lost from the body through osmotic diuresis and vomiting. Hypertonicity causes an increase in plasma osmolarity that causes water and potassium to be drawn from the intracellular space to the extracellular fluid. Proteolysis and glycogenolysis cause an efflux of potassium from the cells. Once potassium is in the extracellular fluid, it is absorbed into the circulatory system. The excess potassium amount, due to loss from the intracellular compartment, is lost from the body through the urinary system. Consequently, the concentration of potassium in the cells is depleted. On the other hand, only excessive potassium amount is excreted through the urinary system and hence normal serum level is maintained.

DKA is associated with osmotic diuresis. The occurrence of diuretic osmotic in DKA is due to hyperglycaemia and hyperketonemia (Craig et al., 2011, p. 128). These conditions lead to increased blood concentrations of glucose and ketone bodies respectively. Elevated amounts of blood glucose and ketone bodies increase the hypertonicity in the cells. Consequently, water is lost from the cells. Hypertonicity in DKA is due to deficiency of insulin that results in increased plasma osmolality (Wolfsdorf et al., 2007, p. 36). The increased osmolarity results to drawing out of water and potassium from the cells into the extracellular spaces from where they are absorbed into the circulatory system. More water is hence found in the circulatory system resulting in its consequential loss through the renal system causing an increase in urine amount. Such high urine volume constitutes osmotic diuresis.

DKA is associated with effects on the movement of potassium in the body. Wolfsdorf et al. (2007, p. 36) claims that the effect of DKA on potassium movement is due to transcellular shifts of the ion in the body. This transcellular shift is due to hypertonicity that causes an increase in the plasma osmolality. The high plasma osmolality causes potassium, alongside water, to move out of the cells into the intracellular compartment. Proteolysis and glycogenolysis enhance this effect of hypertonicity. Proteolysis and glycogenolysis enhance the movement of potassium ions from the cells into the intracellular compartments due to transcellular shifts.

Insulin is essential in the treatment of DKA. It plays a crucial role in correcting hyperkalemia. South Australia Health (2012, p. 9) explains that hyperkalaemia is the presence of high concentration of potassium in the body due to the reduction of the renal function due to overworking of the renal system. Hyperkalaemia results to increased concentrations of potassium levels in the body. High body potassium level causes on neuron polarization. Administration of insulin results in uptake of potassium back into the cells. The re-uptake of sodium into the cells lowers its concentration in the extracellular compartment. Consequently, the body concentration of the potassium reduces resulting in insulin’s corrective effects in hyperkalemia. Therefore, insulin infusion helps in hyperkalaemia correction through their counteractive impact on the movement of potassium from the cells due to DKA.

Nurses have crucial roles in the care of a child with insulin infusion. According to South Australia Health (2012, p.7), the responsibilities of nurses for children with insulin infusion are mainly involved with management and monitoring. Such management and monitoring roles of the nurses in the care of children undergoing through insulin infusion include evaluating biochemical variables such as blood glucose and sodium. Nurses should ensure that the level of these electrolytes remains within the normal level. Moreover, nurses should ensure the development of social confidence of these children. Through their interaction with the children, nurses are expected to create social interactions with them to ensure moral confidence. Nurse are also required to conduct an instrumental assessment of the child’s blood pressure and the electroencephalogram. Such role would be crucial to ensuring that hypertension is checked for due to the interrelation of hypovolemia and hypotension and consequently heart rhythm change. Nurses are also required to offer relevant information to families and other pertinent personnel on dealing with emergency cases. It is also prudent for nurses to ensure frequent examination of the neurological conditions of the child to prevent cerebral oedema.

 

 

Bibliography

BROWNE, T. R., & HOLMES, G. L., 2008. Handbook of epilepsy. Philadelphia, Lippincott Williams & Wilkins.

Craig, M. E. T. S., Twigg, S., Donaghue, K., Cheung, N., Cameron, F., Conn, J., … & Silink, M., 2011. National evidence-based clinical care guidelines for type 1 diabetes in children, adolescents and adults. Canberra: Australian Government Department of Health and Ageing.

Dubé, C. M., Brewster, A. L., Richichi, C., Zha, Q., & Baram, T. Z., 2007. Fever, febrile seizures and epilepsy. Trends in neurosciences, 30(10), 490-496.

Fisher, R. S., Boas, W. V. E., Blume, W., Elger, C., Genton, P., Lee, P., & Engel, J., 2005. Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia, 46(4), 470-472.

JAN, M. M., 2012. Manual of child neurology problem based approach to common disorders. [Dubai, United Arab Emirates], Bentham eBooks.

Karande, S., 2007. Febrile seizures: a review for family physicians. Indian journal of medical sciences, 61(3), 161.

Kelo, M., Martikainen, M., & Eriksson, E., 2013. Patient education of children and their families: nurses’ experiences. Pediatr Nurs, 39(2), 71-79.

Lee, J., Huh, L., Korn, P., & Farrell, K., 2011. Guideline for the management of convulsive status epilepticus in infants and children. British Columbia Medical Journal, 53, 279-285.

NSW Department of Health, 2009. Infants and children: Acute management of seizures – Clinical practice guidelines. 2nd edn, Author, Sydney.

Sadleir, L. G., & Scheffer, I. E., 2007. Febrile seizures. Bmj, 334(7588), 307-311.

Smith, J., & Martin, C., 2008. Paediatric neurosurgery for nurses: evidence-based care for children and their families. Routledge.

South Australia Health, 2012. Diabetic ketoacidosis (DKA) in children: South Australian paediatric clinical guidelines. Government of South Australia, Adelaide, [Online] Available at: < http://www.sahealth.sa.gov.au/wps/wcm/connect/04ac0b8040d0430e975ebf40b897efc8/Diabetic+Ketoacidosis+%28DKA%29+in+Children_Aug2013.pdf?MOD=AJPERES&CACHEID=04ac0b8040d0430e975ebf40b897efc8> Accessed 29 June 2009].

Tatum, W. O., Sirven, J. I., & Cascino, G. D., 2014.  Epilepsy Case Studies Pearls for Patient Care. Cham, Springer International Publishing

The childrens Hospital at Westmead, 2013. Diabetic ketoacidosis: management – chw practice guideline. Author, [Online]. Available at:<http://www.schn.health.nsw.gov.au/_policies/pdf/2008-8061.pdf> Accessed 29 June 2009.

The Royal Childrens Hospital Melbourne, 2015. Clinical practice guidelines: Diabetes Mellitus. Author, [Online]. Available at:<http://www.rch.org.au/clinicalguide/guideline_index/Diabetes_Mellitus/ Accessed 29 June 2009.

Vanelli, M., & Chiarelli, F., 2003. Treatment of diabetic ketoacidosis in children and adolescents. Acta Bio Medica Atenei Parmensis, 74(2), 59-68.

Wolfsdorf, J., Craig, M. E., Daneman, D., Dunger, D., Edge, J., & Lee, W. R. W., 2007.  i SPAD Clinical Practice Consensus Guidelines 2006–2007.Diabetes ketoacidosis. Pediatr Diab, 8, 28-43.