After nearly thirteen years of raising and caring for our alpacas there seems to be no end to experiencing and learning something new. This is our story about a Phrenic Nerve Disorder diagnosis.
History
The first indication something might be wrong with our Remington Steele was an episode of flared nostrils and open mouth breathing on an extremely hot day in the summer '17. I hosed down his belly and it seemed to help so I attributed the episode to heat stress. I observed another episode a few days later and again cooled him off by spraying his belly. Over the course of the next few weeks I noticed he was staying cushed more, interacting with the other juveniles and weanlings far less than normal and seemed disengaged from what was going on around him. On closer observation I noticed although he wasn't breathing through his mouth his breathing was extremely labored. When cushed his back would rise and fall because of the abdominal breathing. It was quite apparent that his breathing was not normal. His weight gain had also stalled and his body score was below normal.
On 10/2/17, at the age of 7 months, he was diagnosed with Phrenic Nerve Disorder. I learned that this was not a common disorder in alpacas and the only suggested “treatment” was to create an environment that was relatively stress free and add Vitamin E to his diet. It was suggested that I separate him from the other juveniles, start feeding him alfalfa because he was underweight and start him on a Vitamin E supplement.
The prognosis at the time was guarded at best. Vitamin E treatment and reduction of stress was the most common approach that could result in a positive outcome. That and the tincture of time…they either relearn how to breathe, grow out of it or both.
My treatment protocol started with putting him in with a group of females that were receiving extra calories through the addition of alfalfa to their diet. This group included his dam. He started nursing and she started producing milk again. This close relationship with his dam seemed to provide him comfort and less stress. I also started him on a Vitamin E supplemental powder added to his pellets. I later switched to liquid Vitamin E also added to his pellets. I pulled him from the three fall shows he was scheduled to attend. Then the waiting began.
You may not have heard of the phrenic nerve before. I certainly hadn’t before I started my research on this condition. This nerve controls the diaphragm muscle, which controls the breathing process and it is one of the many vital bodily functions that is keeping you alive as you read this. When the diaphragm contracts, the chest cavity expands and creates room for inhaled air. Breathing is an involuntary action and something you don’t have to think about. It is the phrenic nerve’s primary function to carry out this process without you having to command your body to do so. When the phrenic nerve is damaged, it can prevent normal breathing.
Although this is an illustration of a human diaphragm it accurately shows the location of the phrenic nerve.The phrenic nerve is actually a twin nerve, with one on the left side and one on the right of the diaphragm. The nerves serve to send signals between the brain and the diaphragm. Breathing is an interesting bodily process because although you usually do not have to think about doing it, you do have the ability to hold your breath or to take a deep breath. The phrenic nerve is responsible for handling these decisions. The phrenic nerves contain motor, sensory, and sympathetic nerve fibers. These nerves provide the only motor supply to the diaphragm. When the nerve is damaged, this control is lost.
The hiccup reflex can be triggered by phrenic nerve irritation, making the diaphragm contract abnormally, resulting in a small intake of air. The most severe impact of phrenic nerve damage is diaphragmatic paralysis, which prevents the patient from being able to regulate breathing on his or her own.
Alpaca Specific Report
Christopher Cebra, in Llama and Alpaca Care, 2014
Diaphragmatic Paralysis
Phrenic nerve degeneration and diaphragmatic paralysis have been reported in the scientific literature and anecdotally in a variety of locations worldwide. The largest study found the disorder only in alpacas less than a year old, but clinical experience suggests that all ages of camelid are susceptible, and many have demonstrated enough normal respiratory function to suggest that this is an acquired lesson. Multiple cases have been identified at specific farms, some sharing a common ancestor. Most clinical cases are bilaterally affected; unilateral cases may exist but may appear normal without extensive examination.
Bilaterally affected camelids usually display an acute onset of progressive dyspnea, with tachyptachypnea, flaring of the nostrils accompanied by expansion of the chest and paradoxic contraction of the abdomen during inspiration, and expansion of the abdomen during expiration. Some appear also to have spinal neurologic signs, including weakness, ataxia, proprioceptive deficits, and knuckling, accompanied by palpable cervical instability in severe cases. Pulmonary sounds are usually normal unless the camelid has aspirated feed or saliva, although the extreme respiratory effort may increase the overall level of noise. Cyanosis and poor body condition may be present but are not consistent findings.
A variety of neurologic conditions, including vertebral body malformation, abscess, and instability, parasitic migration, tumor, degeneration, and trauma may all be causative and require treatment. Vitamin E deficiency may be a factor in nerve degeneration as well.
Treatment efforts have mainly been supportive or directed at an underlying neurologic disease. Supportive treatments could include administration of nasal oxygen or mechanical ventilation. Treatments of the neurologic disease vary and could include anti-inflammatories, antibiotics, antiparasitics, and vitamin E. Prognosis is guarded. Camelids that are in overt respiratory distress or have aspirated are unlikely to thrive. Others appear to tolerate the respiratory compromise and slowly acclimate to it, using the accessor y muscles of breathing to drive their respiratory efforts.
Current Report
Fast forward to 1/29/18...his breathing pattern is normal, he weighs 61.5 lbs which is less than our average 11 month old but his current weight gain is in line with an alpaca his age. He has slowly become more active, is cushing less and is more engaged with his surroundings. He has also stopped seeking comfort through nursing.
His personalized feeding routine is simple and predictable for him. When I come to the barn in the mornings he and his dam move to the gate which opens to an area where they can eat without interruption by the other members of their group. Each receives a combination of Calf Manna and Bar Ale pellets with 3cc’s of liquid Vitamin E on top.
Why is his dam included in this special feeding regimen? Well, genetics has not been widely discussed as a possible cause of Phrenic Nerve Disorder and the genetic factor is as of now unknown. In the meantime, with every day that goes by the future is looking promising for Remmie.
UPDATE 10/1/18
Remmie is 19 months old and all visible signs of his breathing disorder are gone. Although he only weighs 83 lbs his body score is good. He is in with the other yearling males and doing well. We realize he is one of the lucky ones.
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