Neonatal Maladjustment Syndrome - Revision history

Bara at 17:52, 31 July 2012

2012-07-31T17:52:39Z

Bara at 13:34, 5 September 2011

2011-09-05T13:34:29Z

Bara at 13:31, 5 September 2011

2011-09-05T13:31:32Z

Bara: moved Neonatal maladjustment syndrome to Neonatal Maladjustment Syndrome

2011-09-05T13:09:27Z

moved Neonatal maladjustment syndrome to Neonatal Maladjustment Syndrome

HelenD at 15:02, 1 August 2011

2011-08-01T15:02:02Z

HelenD: Created page with "Also know as: '''''NMS — Perinatal Asphyxia Syndrome — Hypoxic ischaemic encephalopathy — Dummy foal — Barker foal ''''' ==Introduction== Neonatal maladjustment syndrome..."

2011-07-24T17:15:04Z

Created page with "Also know as: '''''NMS — Perinatal Asphyxia Syndrome — Hypoxic ischaemic encephalopathy — Dummy foal — Barker foal ''''' ==Introduction== Neonatal maladjustment syndrome..."

New page

Also know as: '''''NMS — Perinatal Asphyxia Syndrome — Hypoxic ischaemic encephalopathy — Dummy foal — Barker foal '''''

==Introduction==
Neonatal maladjustment syndrome is a '''multisystemic disease''' affecting the nervous, cardiovascular, gastrointestinal and renal systems of the neonatal foal. The central nervous signs are noticed first and are the most overt.

Typically, affected foals are normal at birth but show signs within a few hours. Some are obviously abnormal at birth and some take 24 hours to show signs.

A variety of foetal and maternal conditions are associated with NMS:

'''Foetal factors''' include: '''twinning, meconium aspiration, sepsis, prematurity or dysmaturity and severe anaemia'''.

'''Maternal factors''' include: conditions that cause '''hypotension or impaired tissue oxygenation''', maternal surgery or cesaerean section, '''dystocia''' and '''placental abnormalities''' (premature placental separation for example).

Initially, the foal responds to asphyxia by shunting blood away from non-vital organs (gut, kidney, bone..) to vital organs (brain, heart, adrenal glands). Continued asphyxia leads to cerebral ischemia. The brain's stores of glucose are depleted by anaerobic metabolism and glutamate uptake is impaired leading to accumulation and overstimulation of receptors.

Free-radicals are produced which overwhelm the scavenging systems and lead to the release of neurotransmitters and inflammatory mediators.

This goes on to affect all body systems leading to fluid and electrolyte derangements and abnormal acid-base due to central respiratory depression.

==Clinical signs==
Signs can be present at birth but usually develop over the first few hours of life.

Initially, '''behaviour changes''' may be all that is apparent: '''depression''', wandering, loss of affinity for mare, head pressing.

Other possible '''neurologic signs''' include: bruxism, hyperexcitability, '''extensor spasm of the limbs''', head, tail and '''convulsions''' alternating with a semicomatose state. Dysphagia, central blindness, head tilt and nystagmus have also been reported.

Signs of '''trauma''' associated with seizure activity can also be apparent: traumatic blepharitis, eyelid trauma, trauma to bony prominences

'''Respiratory signs''': varying degress of '''tachypnoea and dyspnoea''' and erratic breathing patterns.

'''Cardiovascular signs''': '''tachycardia''', hypotension, or murmurs associated with vavle dysfunction

'''Renal signs''': '''oliguria''' and peripheral oedema if fluid therapy is not adjusted for decreased uring output.

'''Gastrointestinal signs''': ileus, poor feeding, loss of suckle reflex, colic, '''abdominal distension''', gastric reflux and '''diarrhoea'''.

==Diagnosis==
The '''clinical signs''' associated with the condition are usually sufficient to make the diagnosis.

Because the signs of NMS are seen soon after birth, it is often associated with '''failure of passive transfer of antibodies''', which can lead to septicemia.
There are no definitive blood chemistry or white blood cell abnormalities that aid in diagnosis, but these tests are helpful in eliminating other causes of the clinical signs. Other clinical syndromes that can present with similar signs and must be differentiated from NMS include '''hypoglycemia, electrolyte and acid-base derangements, septic meningitis, head trauma, cerebral bleeding, and congenital CNS defects'''.

==Treatment==
'''Intensive supportive care''' is critical for the support of the affected foal. Providing warmth and nutrition is essential. An indwelling nasogastric tube can be placed if the foal is not suckling, and mare's milk should be given.

'''Isotonic fluids with added glucose''' should be given intravenously, and urine output monitored to avoid overhydration.

'''Seizure control''' is imperative, and diazepam should be administered if needed, with long term control using phenobarbital.

'''Respiratory support''' with flow-by oxygen, or positive-pressure ventilation if necessary.

'''Cardiac dysfunction''' can be treated with dopamine to increase cardiac output, and diuretics to reduce oedema.

'''Renal dysfunction''' should be treated with dopamine infusions to increase renal blood flow and urine output.

'''General supportive care''' includes: '''immunologic support''' with plasma infusions if the foal's IgG levels are below 800mg/dl. Antibiotic therapy should be considered because sepsis commonly accompanies ischemic bowel damage, and '''broad-spectrum antibiotics''' should be administered intravenously. '''Anti-ulcer medication''' such as ranitidine and sucralfate are recommended as gastric ulcers are a common complication.

Prevention of further self-trauma by placing a '''padded head-collar''' and paying attention to '''corneal ulceration''' is vital.

==Prognosis==
Prognosis is usually '''good''' for a foal delivered without obvious complications, especially if it is able to stand after delivery and has a normal immunoglobulin concentration. Approximately '''75% of foals with good prognostic indicators survive''' with intensive nursing care. Clinical signs usually stabilise within 3 days but full recovery may take as long as '''2 weeks'''.

A '''poor prognosis''' is associated with foals which have '''concurrent septicaemia''', fail to show neurological improvement within 5 days or suffer from repeat seizures and are persistently comatose.

'''Long-term neurological deficits''' might be seen: unusually docile behaviour, prolonged vision impairment, residual spasticity, recurrent seizures.

==References==
Carleton, C. (2011) '''Blackwell's Five Minute Consult Clinical Companion: Equine Theriogenology''' ''Wiley-Blackwell''

Ogilvie, T. (1998) '''Large animal internal medicine''' ''Wiley-Blackwell''

Synder, J. (2006) '''The equine manual''' ''Elsevier Health Sciences''

Maggs, D. (2008) '''Slatter's fundamentals of veterinary ophthalmology''' ''Elsevier Health Sciences''

[[Category:To Do - Helen]]
[[Category:To Do - Review]]

@@ Line 1: / Line 1: @@
 Also know as: '''''NMS — Perinatal Asphyxia Syndrome — Hypoxic Ischaemic Encephalopathy — Dummy Foal — Barker Foal '''''
@@ Line 77: / Line 78: @@
 {{review}}
 [[Category:Neurological Diseases - Horse]]
 [[Category:Cardiovascular Diseases - Horse]]

← Older revision		Revision as of 13:34, 5 September 2011
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−	Also know as: '''''NMS — Perinatal Asphyxia Syndrome — Hypoxic ~~ischaemic encephalopathy~~ — Dummy ~~foal~~ — Barker ~~foal~~ '''''	+	Also know as: '''''NMS — Perinatal Asphyxia Syndrome — Hypoxic Ischaemic Encephalopathy — Dummy Foal — Barker Foal '''''

	==Introduction==		==Introduction==

← Older revision		Revision as of 15:02, 1 August 2011
Line 64:		Line 64:

	'''Long-term neurological deficits''' might be seen: unusually docile behaviour, prolonged vision impairment, residual spasticity, recurrent seizures.		'''Long-term neurological deficits''' might be seen: unusually docile behaviour, prolonged vision impairment, residual spasticity, recurrent seizures.
		+
		+	{{Learning
		+	\|flashcards = [[Equine Reproduction and Stud Medicine Q&A 01]]
		+	}}

	==References==		==References==

@@ Line 8: / Line 8: @@
 A variety of foetal and maternal conditions are associated with NMS:
-'''Foetal factors''' include: '''twinning, meconium aspiration, sepsis, prematurity or dysmaturity and severe anaemia'''.
+'''Foetal factors''' include: '''twinning, meconium aspiration, sepsis, prematurity or dysmaturity and severe [[:Category:Anaemia|anaemia]]'''.
-'''Maternal factors''' include: conditions that cause '''hypotension or impaired tissue oxygenation''', maternal surgery or cesaerean section, '''dystocia''' and '''placental abnormalities''' (premature placental separation for example).
+'''Maternal factors''' include: conditions that cause '''hypotension or impaired tissue oxygenation''', maternal surgery or cesaerean section, [[Dystocia - Horse|'''dystocia''']] and '''placental abnormalities''' (premature placental separation for example).
-Initially, the foal responds to asphyxia by shunting blood away from non-vital organs (gut, kidney, bone..) to vital organs (brain, heart, adrenal glands). Continued asphyxia leads to cerebral ischemia. The brain's stores of glucose are depleted by anaerobic metabolism and glutamate uptake is impaired leading to accumulation and overstimulation of receptors.
+Initially, the foal responds to asphyxia by shunting blood away from non-vital organs (gut, kidney, bone...) to vital organs (brain, heart, adrenal glands). Continued asphyxia leads to cerebral ischemia. The brain's stores of glucose are depleted by anaerobic metabolism and glutamate uptake is impaired leading to accumulation and overstimulation of receptors.
 Free-radicals are produced which overwhelm the scavenging systems and lead to the release of neurotransmitters and inflammatory mediators.
@@ Line 18: / Line 18: @@
 This goes on to affect all body systems leading to fluid and electrolyte derangements and abnormal acid-base due to central respiratory depression.
-==Clinical signs==
+==Clinical Signs==
-Signs can be present at birth but usually develop over the first few hours of life.
+Signs can be present at birth but usually develop over the first few hours of life. Initially, '''behaviour changes''' may be all that is apparent: '''depression''', wandering, loss of affinity for mare, head pressing. Other possible '''neurologic signs''' include: bruxism, hyperexcitability, '''extensor spasm of the limbs''', head, tail and '''convulsions''' alternating with a semicomatose state. Dysphagia, central blindness, head tilt and nystagmus have also been reported.
-Initially, '''behaviour changes''' may be all that is apparent: '''depression''', wandering, loss of affinity for mare, head pressing.
+Signs of '''trauma''' associated with seizure activity can also be apparent: traumatic [[blepharitis]], eyelid trauma, trauma to bony prominences.
-Other possible '''neurologic signs''' include: bruxism, hyperexcitability, '''extensor spasm of the limbs''', head, tail and '''convulsions''' alternating with a semicomatose state. Dysphagia, central blindness, head tilt and nystagmus have also been reported.
+'''Respiratory signs''' include varying degrees of '''tachypnoea and dyspnoea''' and erratic breathing patterns.
-Signs of '''trauma''' associated with seizure activity can also be apparent: traumatic blepharitis, eyelid trauma, trauma to bony prominences
+'''Cardiovascular signs''' present as '''tachycardia''', hypotension, or murmurs associated with valve dysfunction.
-'''Respiratory signs''': varying degress of '''tachypnoea and dyspnoea''' and erratic breathing patterns.
+'''Renal signs''', '''oliguria''' and peripheral oedema may occur if fluid therapy is not adjusted for decreased urine output.
-'''Cardiovascular signs''': '''tachycardia''', hypotension, or murmurs associated with vavle dysfunction
+'''Gastrointestinal signs''' such as ileus, poor feeding, loss of suckle reflex, colic, '''abdominal distension''', gastric reflux and '''diarrhoea''' can be present.
 ==Diagnosis==
 The '''clinical signs''' associated with the condition are usually sufficient to make the diagnosis.
-Because the signs of NMS are seen soon after birth, it is often associated with '''failure of passive transfer of antibodies''', which can lead to septicemia.
+Because the signs of NMS are seen soon after birth, it is often associated with [[Failure of Passive Transfer|'''failure of passive transfer of antibodies''']], which can lead to [[Septicaemia - Foal|septicemia]].
 There are no definitive blood chemistry or white blood cell abnormalities that aid in diagnosis, but these tests are helpful in eliminating other causes of the clinical signs. Other clinical syndromes that can present with similar signs and must be differentiated from NMS include '''hypoglycemia, electrolyte and acid-base derangements, septic meningitis, head trauma, cerebral bleeding, and congenital CNS defects'''.
@@ Line 46: / Line 43: @@
 '''Isotonic fluids with added glucose''' should be given intravenously, and urine output monitored to avoid overhydration.
-'''Seizure control''' is imperative, and diazepam should be administered if needed, with long term control using phenobarbital.
+'''[[Seizures|Seizure]] control''' is imperative, and diazepam should be administered if needed, with long term control using phenobarbital.
 '''Respiratory support''' with flow-by oxygen, or positive-pressure ventilation if necessary.
@@ Line 54: / Line 51: @@
 '''Renal dysfunction''' should be treated with dopamine infusions to increase renal blood flow and urine output.
-'''General supportive care''' includes: '''immunologic support''' with plasma infusions if the foal's IgG levels are below 800mg/dl. Antibiotic therapy should be considered because sepsis commonly accompanies ischemic bowel damage, and '''broad-spectrum antibiotics''' should be administered intravenously. '''Anti-ulcer medication''' such as ranitidine and sucralfate are recommended as gastric ulcers are a common complication.
+'''General supportive care''' includes: '''immunologic support''' with plasma infusions if the foal's [[IgG]] levels are below 800mg/dl. Antibiotic therapy should be considered because sepsis commonly accompanies ischemic bowel damage, and '''broad-spectrum antibiotics''' should be administered intravenously. '''Anti-ulcer medication''' such as ranitidine and sucralfate are recommended as [[Gastric Ulceration - Horse|gastric ulcers]] are a common complication.
-Prevention of further self-trauma by placing a '''padded head-collar''' and paying attention to '''corneal ulceration''' is vital.
+Prevention of further self-trauma by placing a '''padded head-collar''' and paying attention to [[Corneal Ulcer - Horse|'''corneal ulceration''']] is vital.
 ==Prognosis==
@@ Line 78: / Line 75: @@
 Maggs, D. (2008) '''Slatter's fundamentals of veterinary ophthalmology''' ''Elsevier Health Sciences''
-[[Category:To Do - Helen]]
-[[Category:To Do - Review]]
+{{review}}

← Older revision	Revision as of 13:09, 5 September 2011
(No difference)