By Guest Blogger, Becky Hopfinger, MSN, FNP-C
I come from a strong Neurology background, and for the past 10 years, I have been checking patient’s micronutrient levels without really understanding or recognizing what a huge issue malnutrition really is even in the United States. The UN estimates that around 831 million people living in developing countries still do not have access to enough food to meet their basics needs, 192 children suffer from protein-energy malnutrition, and over 2 billion experience micronutrient deficiencies. (United Nations, 2020) Here in the U.S. our nutritional deficiencies look a little different, and are frequently related to alcohol abuse, dietary habits, and impaired absorption of dietary nutrients secondary to malabsorption syndromes. I wanted to briefly touch on a few of the more common micronutrient deficiencies, how to identify them in your clinic, and how to treat them.
Thiamine Deficiencies
Thiamine deficiencies are frequently seen or related to alcohol abuse. Wernike-Korsakoff syndrome (WKS) is a neurologic disorder characterized by a classic triad of ophthalmoplegia, gait ataxia and confusion. The other symptoms that may accompany this triad are hypotension, hypothermia, cardiac arrhythmias and even coma. The ‘Wernike’ part of the syndrome is related to the thiamine deficiency, whereas Korsafoff psychosis may be seen in other disorders of the nervous system. When a patient presents to our facility with a strong history of alcohol use and part of the triad, we treat. Our practice is to dose with Thiamine 500mg IV TID for three days before decreasing to 100mg daily; this is an aggressive regimen. There are neuropathic changes that occur with WKS including necrosis of both neuronal and oligodendroglial elements in the mammillary bodies, superior cerebellar vermis and hypothalamus. There can also be petechial hemorrhages in the mammillary bodies and periaqueductal gray. Wernike-Korsakoff syndrome should be considered a medical emergency and if suspicion on admission, start thiamine. Also, if you are working in a clinic and have a patient that is a heavy drinker, consider starting on supplementation at home.
Cobalamin (B12) Deficiency
This is one of the most common deficiencies seen in clinical practice. B12 is naturally found in foods including meats, eggs and milk products. The etiology of B12 deficiency may include pernicious anemia, celiac disease, gastric (or ileal) resection, fish tapeworm/parasite infection, inadequate diet (vegan). Coming from a Neurology practice, I order B12 levels on anyone who comes in complaining of neuropathy, and I have found A LOT of deficiencies. The early clinical manifestations of B12 deficiency is tingling and paresthesias in the lower extremities accompanied by pin-and-needles sensation and the perception of muscle weakness. Of note, these early symptoms are because there is demyelination in either the peripheral nerves or the sensory tracts of the spinal cord. As this deficiency progresses patients can develop spastic paraparesis with weakness and greatly increased muscle tone in the lower extremities. The diagnosis of this is relatively easy. It is just a blood test. The lower limit of normal for most labs is around 200pg/ml, although we will treat anything less than 300 pg/ml. Regardless of etiology, treatment should go forth. B12 should be supplemented as IM 1mg for 7 days followed by 1mg IM weekly for a month, and then recheck the level after treatment has concluded. These patients then typically require oral supplementation for much longer depending on cause of deficiency.
Pyridoxine (B6) Deficiency
Pyridoxine assists in the balancing of sodium and potassium as well as promoting RBC production. It is definitely not as common as B12 deficiency and is not part of my usual first line neuropathy work-up. There is a B6 nutritional polyneuropathy found in tuberculous patients. This is thought to be a complication of treatment with isoniazid. The neuropathy is characterized by paresthesia and burning pain of the feet and legs followed by weakness of these parts and lose of ankles reflexes. This can also be seen in frequent use of hydralazines. Pyridoxine deficiency- related polyneuropathy is extremely rare in the absence of these medication (INH and hydralazine).
Copper Deficiency
This is one of the more interesting deficiencies, and one that I have seen only a couple of times in my clinical practice but rewarding when identified. The most common manifestation is that of myelopathy presenting with a spastic gait and prominent sensory ataxia. You may also recognize CNS demyelination, peripheral neuropathy and optic neuropathy. A spinal cord MRI in these patients will show myelopathy and may have increased T2 signal changes most commonly in the dorsal midline of the cervical and thoracic cord. These findings may be reversible with normalization of serum copper levels. Become suspicious of a potential copper deficiency in the patient with worsening spastic, scissoring gait, neuropathy in lower extremities and use of Zinc containing products. Zinc and copper have an inverse relationship. The only people that I have found this deficiency in have been using old or cheap denture cream that is high in Zinc. Treatment for this is daily copper infusions for three days.
Magnesium Deficiency
Magnesium deficiency is a trigger for vasoconstriction and enhances the vascular endothelial injury, thus promoting the development and progression of atherosclerosis and cerebrovascular disease. Amighi et al (2004) demonstrated that hypomagnesium below <0.76mmol/L exhibited a 3.29 fold increase adjusted risk for neurologic vascular events, favoring magnesium substitution therapy in those patients with atherosclerosis as part of a secondary prevention program. Also, involvement in the parkinsonism-dementia complex: significant loss of dopaminergic neurons in SN in 1 year that has been continuous exposed to low Magnesium intake.
The bottom line, is that nutritional deficiencies are very common in any clinical practice, and frequently present with neurologic symptoms. When a patient presents with a new neuropathy, paresthesias or gait ataxia, do not forget to order nutritional labs. Identifying deficiencies can be clinically rewarding for both practitioner and patient, and when identified early can be reversible!
For more clinical tips, check out our post-graduate training and education program, ThriveAP. ThriveAP spends some time covering topics such as this in our year long program geared towards primary care. After NPs and PAs finish school, there is a lot they are expected to know in their first few years of practice. ThriveAP is meant to ease the transition into practice by providing live online webinars for continued didactic learning and mentorship. For more information, please contact info@thriveap.com.
Becky Hopfinger, FNP-C, has been a nurse practitioner for just over 9 years. She started out her NP career in Denver with a Neurosurgery team. With this practice, she worked within the inpatient, outpatient, ED and the OR. She currently works for Washington University in
St. Louis at Barnes Jewish Hospital. This is a Level 1 Trauma Center, and Comprehensive Stroke Center, with 1300 inpatient beds. Her Neurology team is consistently in the top 15 in the country. She is a frequent class speaker for ThriveAP.