Diphallia

Also called Diphallasparatus, penile duplication (PD) or diphallic terata is a rare developmental disorder where a male infant is born with two or more penises. The first reported case was in Bologna; Italy (1609), by Johannes Jacob Wecker, a Swiss female physician and philosopher.

It occurs in 1 out of every 5.5 million males worldwide, and so far only about 100 cases of diphallia have been recorded.

 

Diphallia, Picture credit mamamia.

Diphallia is usually accompanied by other congenital abnormalities like Vertebral (spinal bifida), renal (exstrophy of the bladder, bladder/urethra duplication), hindgut (exstrophy of the cloaca), anorectal (colon and rectosigmoid duplication), skeletal (pubic symphysis diastasis) skeletal muscle abnormalities (ventral hernia) heart muscles abnormalities, etc.

Risk factors/Causes

It is thought diphallia occurs in the fetus between the 23^rd to 35^th day  (3rd to 6th week) of gestation(pregnancy) when an injury; chemical stress, or malfunctioning “homeobox genes” hamper proper function of the caudal cell mass of the foetal mesoderm as the urogenital sinus separates from the genital tubercle and rectum to form the penis.

The embryologic explanation of diphallia is quite obscure, because at no time during normal development is the genital tubercle a paired structure. Reptiles such as snakes and lizards possess a double penis. Moreover, diphallia could represent a teratoid structure or a form of incomplete twinning. Still, none of these explanations is adequate and the wide spectrum of the anomalies cannot be explained by a single hypothesis.

Signs and symptoms

It is believed that no cases are identical as signs and symptoms vary for each patient. It varies from a small accessory penis or duplication of the glans to complete penile duplication.

Generally, it is characterized with two or more penis, both are situated side by side and has equal size, urine passes through both penis, some patient in one penis only, other patient neither of the penis. Some patient is sterile or incapable to produce semen, but the penis will erect if stimulated.

The duplication may be orthotopic or ectopic. Division of the penis may be sagittal or frontal and symmetric or asymmetric, in shape and size.

The urethra shows a range of variations, from functioning double urethras to complete absence of the urethra in each penis. The majority have a single corpus cavernosum in each organ. The meatus may be normal, hypospadias, or epispadia, and the scrotum may be normal or bifid. The testes are normal, athropic, or undescended.

Types

Various classifications for diphallia exist. One classifies it into four types while a recent classification is into two

Classifying Diphallia into four types:

• ·         Diphallia of the glans alone,
• ·         bifid diphallia,
• ·         Complete diphallia.
• ·         Pseudodiphallia.

Classifying diphallia into two types (widely accepted):

• ·         True diphallia; partial duplication or complete duplication.
• ·         Bifid phallus; partial duplication or complete duplication.

True complete diphallia refers to complete penile duplication, each with two corpora cavernosa (body of the penis) and a corpus spongiosum (spongy tissue surrounding the male urethra within the penis). Here both penises are capable of simultaneous erection and ejaculation.

True Partial diphallia; here the duplicate penis is smaller or rudimentary, it corresponds to the term “pseudodiphallia,”. Here the rudimentary or smaller penis may not be capable of erection and ejaculation)

Bifid phallus; when only one corpus cavernosum (body of the penis) is present in each penis. Normal erection in both penises occurs here).

         Complete bifid phallus; when the degree of separation is complete to the base of the shaft

         Partial bifid phallus; when the separation is just to the glans (Tip/cap of the penis).

Diagnosis

Ultrasound is used to help confirm the diagnosis. It detects the number of corpora cavernosum or corpora spongiosum and their accompanying abnormalities. Improved interpretation of anatomical structures has been made possible with the advent of magnetic resonance. Imaging also help in decision making during treatment.

Treatment

Several factors are considered during the treatment of diphallia, these are; medical, ethical and aesthetic factors.

Treatment of diphallia depends on the type of diphallia and the associated anomalies. During treatment of diphallia, it is necessary to individualise each case and also aim at preserving or achieving erectile function, urinary continence, urinary stream and cosmesis.

Surgical Excision of the duplicated noncommunicating penis is reported in many bodies of literature. Penis reconstruction by joining the corporal bodies in each penis in a patient with true complete diphallia has also been reported in some literatures.

Complications

Congenital defects, sterility, erectile dysfunctions, prostatitis, etc.

Prognosis

Infants born with diphallia and its related conditions have a higher death rate from various infections associated with their more complex renal or colorectal systems.

References

R. Mukunda, P. S. Bendre, R. G. Redkar, and S. Hambarde, “Diphallus with anorectal malformation-case report,” Journal of Pediatric Surgery, vol. 45, no. 3, pp. 632–634, 2010

V. C. Varghese and T. U. Sukumaran, “Penile duplication,” Indian Pediatrics, vol. 41, no. 11, p. 1166, 2004

H. S. Bhat, S. Sukumar, T. B. Nair, and C. S. M. Saheed, “Successful surgical correction of true diphallia, scrotal duplication, and associated hypospadias,” Journal of Pediatric Surgery, vol. 41, no. 10, pp. e13–e14, 2006.

M. M. Aboodi and H. A. Al-Jadeed, “Accessory pseudophallus with accessory pseudoscrotum detected during antenatal sonographic scanning,” Journal of Ultrasound in Medicine, vol. 24, no. 8, pp. 1163–1166, 2005.

A. Mirshemirani, F. Roshanzamir, S. Shayeghi, and L. Mohajerzadeh, “Diphallus with imperforate anus and complete duplication of recto-sigmoid colon and lower urinary tract,” Iran Journal of Pediatric, vol. 20, no. 2, pp. 229–232, 2010

S. Priyadarshi, “Diphallus with ectopic bowel segment: a case report,” Pediatric Surgery International, vol. 21, no. 8, pp. 681–683, 2005.

K. Gyftopoulos, K. P. Wolffenbuttel, and R. J. M. Nijman, “Clinical and embryologic aspects of penile duplication and associated anomalies,” Urology, vol. 60, no. 4, pp. 675–679, 2002.

S. Acimi, “Complete diphallia,” Scandinavian Journal of Urology and Nephrology, vol. 38, no. 5, pp. 446–447, 2004.

M. E. Torres, P. J. C. Sanchez, T. A. Aragon, T. V. Camacho, and G. A. Colorado, “Diphalia,” Revista Mexicana de Urología, vol. 69, no. 1, pp. 32–35, 2009.

Wikipedia “Diphallia” Wikipedia 2016.

M. C. de Oliveira, R. Ramires, J. Soares, A. P. Carvalho, and F. Marcelo, “Surgical treatment of penile duplication,” Journal of Pediatric Urology, vol. 6, no. 3, pp. 257-e1–257-e3, 2010

P. Tirtayasa, R. Prasetyo, and A. Rodjani “Diphallia with Associated Anomalies: A Case Report and Literature Review,” Case Reports in Urology Vol. 2013, Article ID 192960, 2013.

Illness Anxiety Disorder Or Hypochondriasis

Illness anxiety disorder (IAD) formerly called Hypochondriasis, Hypochondria, Healthy Anxiety, Illness Phobia or Somatic preoccupation is an overwhelming fear that you have a serious disease based on the misinterpretation of one or more normal bodily signs, even when Doctors can find no evidence of the illness. The disorder is not about the presence or absence of illness, but the psychological reaction.

The term Hypochondrium can be traced back to 400BC when it was used by Hippocrates to describe a region of the abdomen. Back then, it was believed that Hypochondriasis was due to malfunctioning of organs in that region of the abdomen.

This condition is seen in 4-20% of the general population, and in 45% of people with severe psychiatric illnesses. It occurs more in women than men. It occurs at any age, but commonly seen between 36 to 57 years.

 

 picture credit; Anxiety org.

Features

Symptoms of Illness anxiety disorder are not under voluntary control and cannot be explained by physiological causes. 

They include;

Excessive fear, preoccupation or worry over having a serious illness.

The fear persists despite appropriate medical evaluation and reassurance.

The belief is not of delusional intensity and is not restricted to a concern about appearance.

The fear causes clinically significant distress or impairment.

The preoccupation lasts for at least 6 months.

The preoccupation is not explained better by another mood, anxiety, or somatoform disorder.

Physical symptoms are not present or if present, only mild. If another illness is present, or there is a high risk for developing an illness, the person’s concern is out of proportion.

High level of anxiety and alarm over personal health status.

Excessive health-related behaviors (e.g., repeatedly checking body for signs of illness) or shows abnormal avoidance (e.g., avoiding doctors’ appointments and hospitals).

Frequently making medical appointments for reassurance — or, avoiding medical care for fear of being diagnosed with a serious illness.

Avoiding people, places or activities for fear of health risks.

Worrying excessively about a specific medical condition or your risk of developing a medical condition because it runs in the family.

Having so much distress about possible illnesses that it become hard for you to function.

Constantly talking about health and possible illnesses.

Frequently searching the Internet for causes of symptoms or possible illnesses.

The absence of physical findings, after series of medical examinations, supports the diagnosis of hypochondriasis.

Risk Factors/ Causes

Overprotective parents or caregivers,

Family history of hypochondriasis,

Belief,

Excessive health related Internet use,

Mental disorders (Psychosomatic disorders and obsessive compulsive disorders),

Epidemics, pandemics and statistics of outbreaks gives Hypochondriacs an illusion that they have the disease,

Major Stress,

Child abuse/illness,

Neurochemical deficit,

Pathogenesis

Some theories have postulated that neurochemical deficits are responsible for this disorder, such deficits may explain why symptoms overlap, why the disorders are commonly comorbid, and why effective treatments parallel one another (eg, selective serotonin reuptake inhibitors [SSRIs]).

Neurochemicals Implicated in this condition include neurotrophin 3 (NT-3), serotonin (5-HT), etc.

Diagnosis

There is no laboratory or radiologic investigation for the diagnosis of Hypochondriasis or Illness Anxiety Disorder.

Thus diagnosis can only be done can be done using the ICD-10 or the DSM-IV criteria.

The DSM-IV defines hypochondriasis according to the following criteria:

    A. Preoccupation with fears of having, or the idea that one has, a serious disease based on the person's misinterpretation of bodily symptoms.

    B. The preoccupation persists despite appropriate medical evaluation and reassurance.

    C. The belief in Criterion A is not of delusional intensity (as in Delusional Disorder, Somatic Type) and is not restricted to a circumscribed concern about appearance (as in Body Dysmorphic Disorder).

    D. The preoccupation causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.

    E. The duration of the disturbance is at least 6 months.

    F. The preoccupation is not better accounted for by Generalized Anxiety Disorder, Obsessive-Compulsive Disorder, Panic Disorder, a Major Depressive Episode, Separation Anxiety, or another Somatoform Disorder.

The newly published DSM-IV replaces the diagnosis of hypochondriasis with "illness anxiety disorder".

The ICD-10 defines hypochondriasis as follows:

    A. Either one of the following:

            A persistent belief, of at least six months' duration, of the presence of a maximum of two serious physical diseases (of which at least one must be specifically named by the patient).

            A persistent preoccupation with a presumed deformity or disfigurement (body dysmorphic disorder).

    B. Preoccupation with the belief and the symptoms causes persistent distress or interference with personal functioning in daily living, and leads the patient to seek medical treatment or investigations (or equivalent help from local healers).

    C. Persistent refusal to accept medical advice that there is no adequate physical cause for the symptoms or physical abnormality, except for short periods of up to a few weeks at a time immediately after or during medical investigations.

    D. Most commonly used exclusion criteria: not occurring only during any of the schizophrenia and related disorders (F20-F29, particularly F22) or any of the mood disorders (F30-F39).

The Illness Attitude Scale (29 items, 15 min, English only) is used for detection and to assess severity.

The Whitely Index of Hypochondriasis (14 items, 5 min, >14 languages) is used for detection, for rating severity, and for measuring change per interventions.

Differential Diagnosis

Other conditions that should be considered when diagnosing Illness Anxiety Disorder or Hypochondriasis are;

Schizophrenia,

Somatic Symptom Disorders,

Body Dysmorphic Disorders,

Conversion Disorders,

Personality Disorders

Depression,

Anxiety Disorders,

Delusional Disorders.

In this case, the following screening tools are useful in distinguishing Illness Anxiety Disorder from the rest;  

    The Health Anxiety Inventory (HAI) (long version; short version of 14 items, 5 min) reliably distinguishes patients with hypochondriasis from patients with anxiety disorders or healthy controls.

    The Somatoform Disorders Symptom Checklist (65 yes-or-no items, 20 min, >5 languages) screens for hypochondriasis, somatization disorder, BDD, and others.

Treatment

Depending on the severity, patients with illness anxiety disorder may require hospital admission, but mild cases may not.

The following methods are recommended for the management of Hypochondriasis;

Education & Reassurance; here the patient is made to understand the manifestations of hypochondriasis and reassurance is given consistently.

Psychotherapy; using Cognitive behavioral therapy.

Psychosurgery in severe cases,

Lifestyle; Patients with illness anxiety disorders/ hypochondriasis are advised to avoid alcohol, caffeine and nicotine. Regular exercise and quality sleep is also recommended here.

Drugs; this is only recommended in addition to the above methods to prevent complications or reduce symptoms in some cases. The drugs used include; Benzodiazepines (Alprazolam), Antidepressant (Sertraline, Paroxetine, Fluoxetine, Venlafaxine, clomipramine, Imipramine, Citalopram, etc.), Antipsychotics (Pimozide, Risperidone, Olanzapine) or Beta adrenergic receptor blocker (Propranolol). Multivitamin supplements (Vitamin A, B, C, E and D.)

Complications

Social complications; Family and marital issues, Unemployment, bankruptcy from overuse of expensive laboratory or medical facilities,

Complications from investigation procedures,

Suicidal thoughts/ Suicide

Disability

Costly medical bills

Complications from testing procedures

Disability and unemployment

Marital or family problems

Prognosis

It has a good prognosis, especially in patients with high economic status. Sometimes the symptoms last from months to years with long quiescent periods

1/3^rd of the patients improve significantly.

Most children with hypochondriasis recover before adolescence or by early adulthood

References

Ehrlich, S., 2014. Hypochondriasis. University Of Maryland Medical center.

Mayo Clinic, 2015. Illness Anxiety Disorder. Mayo Clinic.

Neziroglu, F., 1998. Hypochondriasis: A Fresh Outlook on Treatment. Psychiatric times.

Olatunji, B., Deacon, B. & Abramowitz, J., 2009. Is hypochondriasis an anxiety disorder? The British Journal of Psychiatry.

Warwick, H., 1998. Cognitive therapy in the treatment of hypochondriasis. Advances in Psychiatric Treatment, 4, pp.285–295.

Xiong, G., 2013. Hypochondriasis. Medscape.

Busy Lifestyle Syndrome (BLS)

This is a real disorder which causes forgetfulness and lack of concentration in people who take in too much information daily.
A good example of Busy Life Syndrome happens when you can't remember why you just walked into the kitchen or room.

Busy Life Syndrome (Picture Credit; TheMomInMemd )

The syndrome was Coined by Scottish researchers to describe this type of memory loss.
It is commonly seen among women; Hard working mums, wives, nurses etc. Can also be seen in Men. Initially it was common among the adults, but now seen in the young.

Causes
According to a Glasgow-based clinical trials company, the syndrome is caused by hectic lives bombarded with information overload from Mobile  Phones, TV, radio, internet, schools, work etc.
The more things we do and see, the more likely we are to forget things.

Another major cause of Busy Life Syndrome is Sleep deprivation; sleeping less than 6hours at night.

Your brain knows you’re unlikely to need to remember a menial task such as going upstairs to get a book in a few hours, so it erases the memory to make room for more important stuffs which you do everyday. Thus sometimes you can't remember why you walked into the room.

Pathophysiology

When you limit the rest time you force the brain to produce excitatory neurotransmitters such as norepinephrine (which is related to the autonomous system to keep you alive), glutamate (which is involved in memory processes, which produces pleasure), dopamine and acetylcholine vitalize handles muscles.
Your body experiences a sense of pleasure that limits us and keeps us stressed, i.e., a situation that is addictive it involves memory loss and lack of concentration.

Signs and Symptoms
Forgetfulness and lack of concentration.

It should be noted that "forgetting" is part of how a healthy brain works. So it should be little surprise that useful things sometimes get deleted among the constant memory-dumping that our brains do as everyday housekeeping.

If your brain did not forget things, you would continually be recalling all kinds of useless information. It would bury you in mental clutter.
Forgetfulness in Busy Life Syndrome should be differentiated from that seen in early onset of Dementia.

The following examples can be seen in Busy Life syndrome
    Forgetting what you went upstairs for.
    Taking several minutes to recall where the car is parked.
    Forgetting to call a friend back while working from home with misbehaving children.
    Putting things down and being unable to find them soon after.
    Forgetting something trivial a friend mentioned the day before.
    Forgetting the name of someone you’ve just met. 
    Briefly forgetting the word for something — the ‘thingamabob’ moment.

The examples below can be seen in early onset of dementia and they are not symptoms of Busy life syndrome.

    Multi-tasking becomes difficult
    Problems negotiating familiar places, such as you regularly can’t find your vehicle in the car park.    
    Forgetting the names of close relatives and friends.
    Problems recognizing faces, colors, shapes and words. 
    Repeating the same question asked half an hour previously.
    Changing personality.
    Finding that you’ve left objects in the wrong place, such as keys left in the lock, and not remembering leaving them there.

Diagnosis
This is purely Clinical using the history. Its symptoms are not are worrisome as those in Early onset of Dementia.

Differential Diagnosis
Alzheimers Disease.

Treatment
Non Medical;Balance activity with Rest, Take breaks, Sleep.
Cut down the less important activities, Prioritize,
Be realistic, Solve one thing at a time.
Perform any recreational activity that demands skills like drawing, singing, dancing etc.
Stay in touch with others.
Cut down on smoking and alcohol intake.
Healthy diet; seafood, fresh nuts, vegetables, fruits etc.
Exercise.

Medical
This is most often not necessary, although some researchers have proposed that the use of low doses of Memantine, a drug for Alzheimers disease, could help But it has not yet been tested.

Restless legs syndrome (RLS) Or Willis-Ekbom disease

This is a Neurological movement disorder characterized by a distressing need or urge to move the legs or arms (akathisia) usually accompanied by an uncomfortable deep-seated sensation in the legs that is brought on by rest; sitting or lying down, relieved by moving or walking, and worse at night or in the evening.
 It may be accompanied by involuntary limb movements while the patient is asleep and can lead to significant physical and emotional disability. Also called Wittmaack-Ekbom syndrome

It was first described by Sir Thomas Willis in 1672 (the founder of clinical neuroscience) who also described of the Circle of Willis.

Restless Leg Syndrome RLS ( Picture Credit; Orthoapnea )

It affect about 2-15% of the world’s population and Caucasians are more prone to this syndrome than African. Can occur at any age and worsens as the patient gets older, Affects women more than men, with a female:male ratio of 2:1.


Mechanism of the disease (Pathophysiology)
Several mechanisms have been implicated;
1) Genetic/run in families; implicated chromosomes are; 12q, 14q, 9p, 20p, 4q, and 17p in autosomal dominant and recessive pattern
2) Low iron levels; as seen in the substantia nigra (brain) of patients with Restless leg syndrome
3) Abnormalities in the central subcortical dopamine pathways


Causes
This depends on the type; Primary or Secondary.

Primary or idiopathic central nervous system (CNS) disorder; which can be familial, following a pattern of autosomal dominant or recessive inheritance with an earlier age of onset (< 45 years) and slower disease progression. Psychiatric factors, stress, and fatigue can worsen symptoms of restless legs syndrome.

Secondary;
Iron deficiency (Particularly); blood ferritin below 50 µg/L (seen in 20% of cases)
peripheral neuropathy
Hypoglycaemia
Parkinson's Disease
Folate or magnesium deficiency
Vitamin B-12 deficiency
Diabetes mellitus
Frequent blood donation        
Rheumatoid arthritis
Uremia
End-stage renal disease (seen 25-50% of patients with End stage renal disease & may improve after kidney transplantation)
Hemodialysis
Pregnancy (seen in 25-40% of pregnant women & usually subsides within a few weeks after delivery).
Drugs; Alcohol, Caffeine, Beta blockers, Diphenhydramine, Lithium, Antidopaminergic medications, Tricyclic antidepressants, Selective serotonin reuptake inhibitors (SSRIs), Serotonin-norepinepherine reuptake inhibitors (SNRIs) etc.
   


Signs and Symptoms

• An urge to move, usually due to uncomfortable sensations that occur primarily in the legs, but occasionally in the arms or elsewhere uncomfortable.The sensations could be described as painful, antsy, electrical, creeping, itching, pins and needles, pulling, crawling, and numbness, internal itch sensation. Some people have little or no sensation, yet still have a strong urge to move. This sensation is relieved (temporary and partially) by movement mostly Walking. It is Worsened by relaxation (Sitting or lying down) and the severity depends on the duration of the rest.Symptoms worsen in the night and in the morning, though some experience it throughout the day and night; Others experience it only in the morning or only at night.

• Sleep disturbance; About 85% of this patients have periodic movements during sleep, usually involving the legs (periodic leg movements of sleep [PLMS]). PLMS are characterized by involuntary, forceful dorsiflexion of the foot lasting 0.5-5 seconds and occurring every 20-40 seconds throughout sleep, resulting in difficulty falling asleep at night.

• Daytime fatigue

Diagnosis
This is mostly from the history.
The International Restless Legs Syndrome Study Group (IRLSSG) updated its diagnostic criteria in 2012. The current IRLSSG criteria are nearly identical to the DSM-5 criteria.
According to the IRLSSG, Restless legs syndrome (RLS) is diagnosed by ascertaining a syndrome that consists of all of the following features:

(1)An urge to move the legs usually but not always accompanied by or felt to be caused by uncomfortable and unpleasant sensations in the legs.

(2)The urge to move the legs and any accompanying unpleasant sensations begin or worsen during periods of rest or inactivity such as lying down or sitting.

(3)The urge to move the legs and any accompanying unpleasant sensations are partially or totally relieved by movement, such as walking or stretching, at least as long as the activity continues.

(4)The urge to move the legs and any accompanying unpleasant sensations during rest or inactivity only occur or are worse in the evening or night than during the day.

(5)The occurrence of the above features are not solely accounted for as symptoms primary to another medical or a behavioral condition (e.g., myalgia, venous stasis, leg edema, arthritis, leg cramps, positional discomfort, habitual foot tapping).

Specifier for clinical significance of RLS
The symptoms of RLS cause significant distress or impairment in social, occupational, educational, or other important areas of functioning by the impact on sleep, energy/vitality, daily activities, behavior, cognition, or mood.

Specifiers for clinical course of RLSf

(A)Chronic-persistent RLS: symptoms when not treated would occur on average at least twice weekly for the past year.

(B)Intermittent RLS: symptoms when not treated would occur on average <2/week for the past year, with at least five lifetime events.

Note that ;
i) Sometimes the urge to move the legs is present without the uncomfortable sensations and sometimes the arms or other parts of the body are involved in addition to the legs.

ii) For children, the description of these symptoms should be in the child’s own words.

iii) When symptoms are very severe, relief by activity may not be noticeable but must have been previously present.

iv) When symptoms are very severe, the worsening in the evening or night may not be noticeable but must have been previously present.

v) These conditions, often referred to as “Restless Legs Syndrome mimics,” have been commonly confused with Restless Legs Syndrome, particularly in surveys because they produce symptoms that meet or at least come close to meeting criteria 1–4 above. The list here gives some examples that have been noted as particularly significant in epidemiological studies and clinical practice. However, Restless Legs Syndrome may also occur with any of these conditions, requiring a clear delineation of the Restless Legs Syndrome feelings from the other sensations.

vi) The clinical course criteria do not apply for pediatric cases or for some special cases of provoked Restless Legs Syndrome such as pregnancy or drug-induced Restless Legs Syndrome, in which the frequency may be high but limited to the duration of the provocative condition.

Differential Diagnosis
Other conditions that present like Restless Leg syndrome include;
    Akathisia
    Neuropathy
    Nocturnal leg cramps
    Painful legs and moving toes
    Vascular disease
    Radiculopathy

Investigations
A complete iron panel; iron levels, ferritin, transferrin saturation, and total iron binding capacity.
Complete blood count (CBC)
Blood urea nitrogen (BUN)
Also check for the following;
Creatinine
Fasting blood glucose
Magnesium
Thyroid-stimulating hormone (TSH)
Vitamin B-12 & Folate
Needle electromyography (EMG) and nerve conduction studies should be considered if polyneuropathy or radiculopathy is suspected on clinical grounds, even if the results of the neurologic examination are apparently normal.

Treatment
Medical
For primary Restless Leg Syndrome, drug therapy is only for symptomatic relieve; curative treatment is possible only for secondary Restless Leg Syndrome.

A Task Force of the International Restless Legs Syndrome Study Group (IRLSSG) developed evidence-based guidelines for long-term pharmacologic treatment of RLS which are as follow;

· Pregabalin - Effective for up to 1 year in treating RLS (evidence level, A).

· Pramipexole, ropinirole, and rotigotine - Effective for up to 6 months in treating Restless Leg Syndrome (evidence level, A)

· Gabapentin enacarbil (1 year), pramipexole (1 year), ropinirole (1 year), levodopa (2 years), and rotigotine (5 years) - Probably effective in treating Restless Leg Syndrome for durations ranging from 1 to 5 years (evidence level, B)

· Pergolide and cabergoline - Because of associated safety concerns, not to be used in treating Restless Leg Syndrome unless the benefits clearly outweigh the risks

The IRLSSG Task Force recommends either a dopamine-receptor agonist or an alpha2-delta calcium-channel ligand as first-line treatment therapy for RLS in most patients, with the choice of medication depending on symptom severity, cognitive status, history, and comorbid conditions.

All patients with low iron levels (ferritin < 50 ng/mL) should receive supplemental iron therapy. In iron deficiency, 325 mg of ferrous sulfate may be given with 250 mg of vitamin C. Absorption is increased by taking this on an empty stomach and waiting 60 minutes before eating. Parenteral iron may also have a role in the treatment of RLS secondary to iron deficiency anemia.

Children with low serum ferritin (< 50 ng/mL) should be treated with supplemental iron therapy. Dopaminergic therapy was found to be effective in small series in children with RLS.

Non-Medical Therapy; 

• Sleep hygiene measures should be recommended to all patients. Moreover, patients with mild RLS who are sensitive to caffeine, alcohol, nicotine, selective serotonin re-uptake inhibitors [SSRIs], diphenhydramine, or dopamine antagonists should avoid these substances.

• Exercise may be helpful for some patients; however, physical measures are only partially or temporarily helpful and should be avoided before bedtime. Some patients benefit from different physical modalities before bedtime, such as a hot or cold bath, a whirlpool bath, limb massage, or vibratory or electrical stimulation of the feet and toes.

Non-pharmacologic management and sleep hygiene measures are the treatments of choice in children. A regular sleep/wake schedule and the elimination of stimulating activity and caffeine before bedtime are important measures.

Prognosis
Over time, the symptoms worsen in about 2/3rd of this patients, ranging from mild to intolerable. In addition to being experienced in the legs, sensations also may occur in the arms or elsewhere.
By the age of 50 symptoms usually progresses to severe, daily disruption of sleep leading to decreased daytime alertness. RLS has been associated with reduced quality of life in cross-sectional analysis.
Patients with RLS and periodic leg movements of sleep (PLMS) may be at increased risk for hypertension because PLMS is associated with an autonomic surge and an increase in blood pressure.
Patients may also be more prone to headaches (migraine and tension-type). The headaches are probably secondary to disturbances in sleep associated with RLS and PLMS.

Learning and memory difficulties have also been associated with RLS, presumably secondary to disrupted nocturnal sleep.

Restless Leg Syndrome ( Picture Credit; Fooyoh )

REFERENCES

Abetz L, Allen R, Follet A, et al. Evaluating the quality of life of patients with restless legs syndrome. Clin Ther. Jun 2004;26(6):925-35.

Berger K, Luedemann J, Trenkwalder C, et al. Sex and the risk of restless legs syndrome in the general population. Arch Intern Med. Jan 26 2004;164(2):196-202.

Cesnik E, Casetta I, Turri M, Govoni V, Granieri E, Strambi LF, et al. Transient RLS during pregnancy is a risk factor for the chronic idiopathic form. Neurology. Dec  2010;75(23):2117-20

Ekbom K, Ulfberg J. Restless legs syndrome. J Intern Med. Nov 2009;266(5):419-31.

Garcia-Borreguero D, Kohnen R, Silber MH, Winkelman JW, Earley CJ, Högl B, et al. The long-term treatment of restless legs syndrome/Willis-Ekbom disease: evidence-based guidelines and clinical consensus best practice guidance: a report from the International Restless Legs Syndrome Study Group. Sleep Med. Jul 2013;14(7):675-84

Giannaki CD, Hadjigeorgiou GM, Karatzaferi C, Maridaki MD, Koutedakis Y, Founta P, et al. A single-blind randomized controlled trial to evaluate the effect of 6 months

of progressive aerobic exercise training in patients with uraemic restless legs syndrome. Nephrol Dial Transplant. Aug 2013;

Godau, Jana; Klose, Uwe; Di Santo, Adriana; Schweitzer, Katherine; Berg, Daniela (2008). "Multiregional brain iron deficiency in restless legs syndrome". Movement Disorders 23 (8): 1184–1187.

Hening WA. Restless Legs Syndrome. Curr Treat Options Neurol. Sep 1999;1(4):309-319.

International Restless Legs Study Group. IRLSSG Diagnostic Criteria for RLS (2012). www.irlssg.org. Updated 2013. Accessed April, 2015

Kutner NG, Zhang R, Huang Y, Bliwise DL. Racial differences in restless legs symptoms and serum ferritin in an incident dialysis patient cohort. Int Urol Nephrol. Jan 2012.

"Restless legs syndrome: detection and management in primary care. National Heart, Lung, and Blood Institute Working Group on Restless Legs Syndrome". American family physician 62 (1): 108–14. 2000

Trenkwalder C, Hogl B, Winkelmann J. Recent advances in the diagnosis, genetics and treatment of restless legs syndrome. J Neurol. Apr 2009; 256(4):539-53.

Aerosinusitis or Barosinusitis

This is painful inflammation or edema of the sinuses (especially the frontal sinuses), which may be accompanied by bleeding and preceded by an upper respiratory tract infection or acute exacerbation of allergies. It occurs when flying in an aircraft or during deep sea diving and is due to non-equilibration or pressure differences of the internal (within the sinuses) and  the external atmospheric pressure.
It can also be called Barotrauma or Sinus squeeze

Paranasal Sinusis (Picture Credit ;Central Coast ENT)

It occurs about 3-4 episodes per 100,000 exposures, has no racial or gender predilection & rarely reported in children, as the frontal sinuses are not fully developed.

Risk Factors

• Upper respiratory tract infection
• Allergy
• Ambient pressure changes or rapid altitude changes; High altitude flyers, high-performance aircraft, military pilots, Deep-sea Divers, Sport divers, Caisson or tunnel workers.
• Nasal polyps
• Anatomic abnormalities of the nose
• Smoking; in children and older adults
• Flying in an airplane after diving

Pathophysiology

Normally,for ventilation and mucocilliary clearance to occur, the sinuses drain through a small ostia into the nasal cavity. This leads to an equilibrium in pressure between the sinuses and the external atmosphere. But when this opening/ostia is blocked by mucousal thickening (as seen in allergies, upper respiratory tract infection, nasal polyps etc) there is no free flow of air (or equilibrium) between the sinuses and the nasal cavity. Following a rapid change in altitude (during flight or diving), there may be compression on the fifth cranial nerve, thus resulting in the Severe frontal headache which is experienced during Aerosinusitis.

There are 2 types of acute barotrauma: The Squeeze and The Reverse Squeeze.
Squeeze occurs during descent; when the sinuses contracts producing a negative pressure, air is trapped causing a partial vacuum within the sinus cavities. If the vacuum is great enough, it causes rupture of the blood vessels in the sinus cavities and may tear the membrane lining. The pain involved is usually sharp, piercing, and severe; upon descent the sinuses may fill with fluids/transudates, and there may be nose bleeding.

The Reverse squeeze occurs during ascent, when the sinuses expand and the pressure increases within the sinuses, but the air within the sinuses cannot escape to the nasal cavity because the ostia is blocked. The expanded sinuses compresses on the fifth cranial nerve, producing frontal headache.

This pathophysiology can be explained by Boyle's law, which states that "the volume of a gas is inversely proportional to the pressure on it, when temperature is constant (V = CT/P)".


Grades
Weissman grading of aerosinusitis;
    Grade I; mild transient sinus discomfort without visible features on X-ray.
    Grade II; pain lasting up to 24 hrs, with some mucosal thickening on X-ray, Serosanguinous Rhinorrhea.
    Grade III; Severe pain lasting more than 24 hrs with X-ray film showing severe mucosal thickening or opacification of the affected sinus; subsequent sinusitis may be observed. Epistaxis, Hematoma and mucosal avulsion.

Signs and symptoms
The predominant symptom is sudden & sharp facial pain or headache during ascent or descent
Mild
 mild pain just above the brow, rarely referred to other regions of the head
 rarely or occassionally have nose bleeding (epistaxis)
Severe
Sudden, sharp and severe pain in the face,and refered to other regions of the head (retroorbital, midface etc).
Accompanied by Nose bleeding (Epistaxis)

Diagnosis
This is Clinical; positive history of the risk factors and symptoms following exposure.
Radiological examination is not really necessary for the diagnosis as this can be done from the history and physical examination. However it may be useful for grading of the Barotrauma.

X-Ray shows mucosal thickening.
CT scanning shows the sinuses involved, extent of any hematoma, and mucosal thickening. It can also suggest the predisposing factor.

Differential Diagnosis
Nasal Polyposis
Turbinate Dysfunction
Seasonal or perineal allergic rhinitis
Nasal septal deviation
Concha bullosa

Prevention
Use a nasal decongestant before ascending or descending,
Avoid rapid descent or ascent,
Avoiding airplanes or scuba diving when you have an upper respiratory infection,
Use valsalva maneuvers to help equalize pressure in the sinuses and inner ears,
Chew gum during take off or landing,
Yawn during flight,
Use filtered earplugs,
Be properly trained before diving.
To prevent pulmonary barotrauma, do not hold your breath during ascent (divers).
Don’t smoke before diving.
Don’t stay under the water at greater depths for so long.
Avoid flying or going to a higher altitude within 24 hours after diving.

Treatment
Most often, immediate treatment is not always possible, but ideally the following should be done;
Immediately return to the altitude which the symptom started (this may be difficult if it happens in a commercial flight) apply topical nasal decongestants before ascending/descending slowly.
Treatment should be aimed at; pain control, ventilation and to prevent infection.
Pain control with analgesics. Depending on the severity, nacortics can be prescribed. Avoid NSAIDs as it may worsen the Hematoma
Ventilation can be aided with nasal decongestants; oral or nasal spray,
Prevent secondary infections using broad spectrum antibiotics (e.g cephalosporins) because the accumulated transudates, hematoma and damaged mucosa can serve as a medium for bacterial growth.
Surgery can be done for very severe cases lasting more than 24hrs and when the analgesics fail to relieve pain. The following surgeries can be performed; Septoplasty, turbinectomy,balloon sinuplasty, Endoscopic sinus surgery etc.


Complications
 Long-term or permanent hearing loss,
 Ear infection,
 Perforated eardrum.
 Orbital cellulitis,
 Meningitis,
 Brain abscess,
 Osteomyelitis (Pott's puffy tumour when the frontal bone is affected)
 Cavernous sinus thrombosis.

Paranasal Sinusis (picture Credit; Pediatrics ENT Associates)

Notes
1) American Academy of Otolaryngology—Head and Neck Surgery; Barosinusitis

2) Brubakk, A. O.; T. S. Neuman (2003). Bennett and Elliott's physiology and medicine of diving, 5th Rev ed. United States: Saunders Ltd. p. 800. ISBN 0-7020-2571-2

3) Encyclopedia Britannica; Aerosinusitis

4) Fitzpatrick DT, Franck BA, Mason KT, Shannon SG (1999). "Risk factors for symptomatic otic and sinus barotrauma in a multiplace hyperbaric chamber". Undersea Hyperb Med 26 (4): 243–7. PMID 10642071.

5) Gunn DJ, O'Hagan S. Unilateral optic neuropathy from possible sphenoidal sinus barotrauma after recreational scuba diving: a case report. Undersea Hyperb Med. Jan-Feb 2013;40(1):81-6.

6) Hanna HH, Tarington CT. Otolaryngology in aerospace medicine. In: DeHart RL, ed. Fundamentals of Aerospace Medicine. Philadelphia: Lippincott Williams & Wilkins; 1985:520-530.

7) Kristin Hayes, Preventing Sinus Squeeze, Ent About. Updated October 30, 2014.

8) Medical Dictionary; Segen's Medical Dictionary. © 2012 Farlex,

9) Medscape; Aerosinusitis

10) US Navy Diving Manual, 6th revision. United States: US Naval Sea Systems Command. 2006.

11) Wikipedia; Aerosinusitis

Harlequin ichthyosis or Harlequin baby

A rare autosomal recessive disease of infants in which the baby is encased in a massive, horny shell of dense, plate-like scale (hyperkeratotic ‘cocoon’) with deep cracks (fissures), accompanied by contraction abnormalities of the eyes (ectropion), turning outwards of a lip (eclabium), and flattened ears.
Also known as; Harlequin-type ichthyosis, keratosis diffusa fetalis, Harlequin fetus

It is the most severe form of autosomal recessive congenital ichthyosis where the dermis to be around 10 times thicker than normal.

Harlequin Baby ( Picture credit; Parakovacs )

It was first Described in 1750 by Rev. Oliver Hart, a cleric from South Carolina. The term "harlequin" derives from the newborn's facial expression, the triangular and diamond-shaped pattern of hyperkeratosis.

It has an incidence rate of less than 1/1,000,000. It has no racial predilection and affects male and female equally.

Risk Factors

• Family History of Ichthyosis or other Severe Skin disorders
• Consanguineous Couples; Marrying a blood relation
• Having another child with ichthyosis ( 25% risk of recurrence)

Pathophysiology

In Harlequin ichthyosis there is Mutations of ABCA12; The gene which is responsible for fat(lipids) transport from lamellar granules to the apical surface of granular layer keratinocytes (spaces between the cells in the skin’s uppermost layer). Thus this mechanism becomes defective resulting in a severe dyskeratosis, caused by defective lipid metabolism; as the lipids are not transported, the stratum corneum is up to 30-fold thicker than the stratum malpighii & the stratum granulosa is decreased to a one-cell layer or absent.

Signs & Symptoms
History of previous intrauterine or neonatal death,
Decreased fetal movements or intrauterine growth retardation noted during the pregnancy,
Preterm delivery,
Bleeding at birth,
Severely thickened & hyperkeratotic skin which is scale-like and shiny with deep cracks/fissures.
Everted eyelids (Ectropion) with dryness of the cornea
The Nose and Ears may be poorly formed or absent
The Lips are retracted (Eclabium)
Sparse hair distribution, alopecias
Poor movement in the joints & contractures
Failure to thrive
Dehydration as a result of fluid loss from the cracked skin.
Hyperthermia due to thickened skin and absence of sweating
Respiratory distress and respiratory failure following poor chest wall expansion

Diagnosis
This is purely clinical, the risk factors, signs and symptoms should be noted.
Prenatal diagnosis, using amniotic fluid sample at 17weeks of gestation, especially for fetuses with positive family history
Prenatal 2D or 3D ultrasonography shows; a large and gaping mouth, aplasia of the nose, abnormal limbs, and bulging eyes; all features of Harlequin ichthyosis.
Genetic testing for mutations in the ABCA12 gene
Full Blood Count; may show decreased heamoglobin, increase White blood cells
Blood culture for infections
Serum Electrolytes Urea and Creatinine may be abnormal due to dehydration.
Chest X-Ray in respiratory distress.
Skin Biopsy for histological studies.

Differential Diagnosis

Self-healing lamellar ichthyosis of the newborn.
Congenital ichthyosiform erythroderma.
Collodion baby.
Lethal restrictive dermopathy.
Infantile systemic hyalinosis.
Neu-Laxova syndrome.

Treatment
The management of Harlequin Ichthyosis is multidisciplinary as well as supportive. It involves the; Neonatologist, Ophthalmologist, Dermatologist, Dietician, Plastic Surgeon, Psychologists etc.
Intravenous access may be difficult here, thus umbilical cannulation is recommended.
Supportive measures include; 

• Monitoring the patient in a Neonatal Intensive care unit,
• The use of Humidified incubator (to maintain body temperature and to prevent the skin from cracking).
• Rehydration
• Lubricating the Cornea with Ophthalmic lubricants
• Emollients can be applied liberally to the skin
• Antibiotics to help prevent infection & sepsis
• Retinoids; Oral(Isotretinoin or acitretin) and Topical Retinoids (Tazarotene) to accelerate shedding of the skin scales.

Complications
Impaired vision
Delayed developmental milestones
Fulminant Sepsis
Failure to thrive
Respiratory failure
Renal failure

Prognosis
The mortality rate for harlequin ichthyosis is high, close to 50%. However, following the discovery of Isotretinoids the prognosis is improving.
Presently, the Oldest surviving person with Harlequin ichthyosis is Nusrit "Nelly" Shaheen, 30years old, from West Midlands in Britain. She was born in 1984,

Harlequin Ichthyosis (Picture Credit; ObGyn)

NOTES

1) Akiyama M. ABCA12 mutations and autosomal recessive congenital ichthyosis: a review of genotype/phenotype correlations and of pathogenetic concepts. Hum Mutat. Oct 2010;31(10):1090-6.

2) Chua CN, Ainsworth J. Ocular management of harlequin syndrome. Arch Ophthalmol. Mar 2001;119(3):454-5

3) First foundation for Ichthyosis and related skin types | Harlequin Ichthyosis

4) Ichthyosis Support Group | harlequin-ichthyosis

5) Kelsell DP, Norgett EE, Unsworth H, et al. Mutations in ABCA12 underlie the severe congenital skin disease harlequin ichthyosis. Am J Hum Genet. May 2005;76(5):794-803

6) Koochek A, Choate KA, Milstone LM. Harlequin Ichthyosis: Neonatal Management and Identification of a New ABCA12 Mutation. Pediatr Dermatol. Mar 2014;31(2):e63-4.

7) Lefevre C, Audebert S, Jobard F, et al. Mutations in the transporter ABCA12 are associated with lamellar ichthyosis type 2. Hum Mol Genet. Sep 15 2003;12(18):2369-78.

8) Medscape; Harlequin Ichthyosis

9) Liu RH, Becker B, Gunkel J, Teng J. Rapid improvement in digital ischemia and acral contracture in a collodion baby treated with topical tazarotene. J Drugs Dermatol. Jun 2010;9(6):713-6.

10) Orphanet; ORPHA457, Harlequin ichthyosis

11) Rajpopat S, Moss C, Mellerio J, et al. Harlequin ichthyosis: a review of clinical and molecular findings in 45 cases. Arch Dermatol. Jun 2011;147(6):681-6.

12) Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN 1-4160-2999-0

13) Wikipedia; Harlequin Ichthyosis

Maggot Therapy

Also called; Biodebridement, Maggot debridement therapy (MDT) or Larval therapy.

This is the controlled, therapeutic application of live blowfly (Lucilia sp) larvae ("maggots") into non-healing wounds to to aid in wound debridement (cleaning), disinfection and/or healing.It can also be termed "Therapeutic Myiasis" as we recall that maggot infestation on a living vertebrate host is called "myiasis".

Maggot Therapy (Picture Credit; Science Open)

"Despite our low cultural esteem for maggots, more and more clinicians and patients are turning to medicinal maggots for assistance with their wound healing. For most, the drawbacks of maggot therapy pale in comparison to the remarkable efficacy in treating even the most recalcitrant wounds"- Ronald A. Sherman,

Though It sounds medieval, Maggot therapy is an accepted part of modern medicine as Debridement is an essential component of wound care; the presence of devitalized tissue can impede the healing process.

History Of Maggot Therapy
The beneficial effects of therapeutic myiasis were first observed during the Napoleonic war by Larrey, who noted that soldiers whose wounds had become infested with maggots had an improved prognosis.
William Baer, while at Johns Hopkins University in Baltimore, Maryland, may have been the first person to have intentionally applied larvae to wounds in order to induce wound healing. During the late 1920's, he identified certain species, raised them in the laboratory, and used their larvae to treat several children with osteomyelitis and soft tissue infections. He presented his findings at a surgical conference in 1929. Two years later, after treating 98 children, his findings were published posthumously.
Throughout the 1930’s Maggot Therapy was performed routinely by Doctors until the discovery of new antibiotics and surgical techniques that came out during World War II. Maggot therapy was occasionally used during the 1970's and 1980's, but only when antibiotics, surgery, and modern wound care failed to control the advancing wound.

The emergence of antibiotic-resistant strains of bacteria such as methicillin resistant Staphylococcus aureus (MRSA) and the curiosity of researchers prompted the reemergence of larval therapy during 1970's & 1980's . As a treatment it meets the demands of clinical governance, being not only beneficial to the patient, but also being proven to be more cost-effective.

In January 2004, the U.S. Food and Drug Administration (FDA) granted permission to produce and market Medicinal maggots. Same year the British National Health Service (NHS) gave approval for maggot therapy. Presently, about 30 countries around the world are using Maggot therapy; In Africa, it is being used in Kenya & South Africa. In European Union, Canada, Japan, maggots are classified as medicinal drugs, needing a full market license.

Mechanism Of Action
Debridement; The maggots secrete a broad spectrum of digestive juice (collagenases, proteolytic enzymes, serine proteases) that selectively liquefy and absorb only necrotic tissue (extracorporeal digestion). Also Mechanical Debridement by the specific mandibles or “mouth hooks” of the maggots and their rough body which both scratch the necrotic tissue.

Disinfection; It was discovered that secretions from maggots (allantoin, urea, phenylacetic acid, phenylacetaldehyde, calcium carbonate, proteolytic enzymes, etc) have broad-spectrum antimicrobial activity, and microbes not killed by these secretions are subsequently ingested and lysed within the maggots. Maggot secretions have been found to dissolve biofilms.

Stimulation of healing; The alkalinity of maggot-treated wounds, along with the isolated allantoin and urea-containing compounds is responsible for wound healing. In fact, today, allantoin and urea are components of many cosmetics. Maggot secretions also;
 -stimulates the proliferation of fibroblasts and endothelial tissue ,
 -increases angiogenesis,
 -enhances fibroblast migration over model wound surfaces.
Using remittance spectroscopy to evaluate patients before and after maggot therapy, Wollina and colleagues found that vascular perfusion and tissue oxygenation surrounding the wound actually increased following maggot therapy. Zhang and colleagues are currently seeing evidence that maggot extracts may even stimulate the growth of neural tissue.

Uses/Indication

• Diabetic Foot Ulcer
• For debriding non-healing necrotic skin and soft tissue wounds including;

               -pressure ulcers,
               -venous stasis ulcers,
               -neuropathic foot ulcers,
               -non-healing traumatic or post-surgical wounds
               -infectious

• In diabetic and non-diabetic subjects for wound bed preparation prior to surgical closure.

Dosage & Administration
Maggots are applied to the wound at a dose of 5–10 larvae per square centimeter of wound surface area and are left within their dressing for 48–72 hrs. At that point they are satiated (as evidenced by increase in size), finished working, and can be removed and safely disposed.

Maggot therapy being a controlled therapeutic myiasis (maggot infestation on a live host) is controlled by;

selecting a safe and effective species and strain,

• chemical disinfection to make the maggots germ-free (sterile maggots),
• containing the maggots within special dressings(e.g maggot confinement dressings; Le Flap™,Biobag™ ) that prevent them from leaving the wound unescorted,
• quality control measures throughout the breeding and production processes.

Not all species are safe and effective. The maggots cleared for marketing in the United States belong to the (currently named) LB-01 strain of Phaenicia (Lucilia) sericata.

Advantages Of Maggot Therapy

1. Takes about 15-30 minutes to apply a secure dressing to keep the maggots in place
2. Low cost of treatment
3. Excellent safety record.
4. Simple enough that non-surgeons can use it to provide thorough debridement when surgery is not available or is not the optimal choice
5. Provide surgical quality debridement as an outpatient or in the home
6. Provides treatment for wounds infected by strains of methicillin resistant Staphylococcus aureus (MRSA)
7. As larvae are typically applied for 3 days, wounds are disturbed less frequently than conventional dressings that require changing everyday

Disadvantages

1. Bacteria like Pseudomonas aeruginosa, Escherichia coli, Enterococcus, Proteus are not attacked by maggots and in case of Pseudomonas even the maggots are in danger. Consequently, using maggots alone might lead to a change of bacteria cultures on the wound.
2. Ineffective in case of highly discharging or dried wounds
3. Medicinal maggots are highly perishable and susceptible to transportation problems and delays. Young, starving larvae require food, water, and oxygen, and they are temperature sensitive. Therefore they must be shipped by overnight courier, and their arrival should be timed no more than 24 h before their application to the wound. Delivery delays and exposure to extreme temperatures decrease their survival.
4. Occasionally the maggots may escape from the wounds and 1–2 weeks later become adult flies (“used maggots” and flies are essentially mobile fomites)
5. Local discomfort, itching, unaesthetic appearance to the patient along with cost of the therapy and short half life of maggots
6. It cannot be used in open wounds of body cavities as the environment is not suitable
7. Negative perception with which it is regarded by both patients and doctors; The 'yuk factor'

Side Effects
Minor bleeding,Pain,
Excessively induced exudates,
Increased body temperature,
Flu-like symptoms,
Allergic reaction,
Skin maceration
Discomfort.

Contraindications
Patients refusal.

Alternative Therapies

• Biotherapies like; apitherapy (application of honey) and application of leeches.
• Sonotherapy (with use of ultrasounds)
• Hydrosurgical therapy (with use of water jets)
• Hyperbaric Oxygen Therapy (HBOT)

Medical Maggots™ (Picture Credit; Live science)

Maggot Debridement Therapy (Picture Credit; btmcl)

NOTES
1) A. J. Horobin, K. M. Shakesheff, S. Woodrow, C. Robinson, and D. I. Pritchard, “Maggots and wound healing: an investigation of the effects of secretions from Lucilia sericata larvae upon interactions between human dermal fibroblasts and extracellular matrix components,” The British Journal of Dermatology, vol. 148, no. 5, pp. 422–933, 2003.

2) A. G. Smith, R. A. Powis, D. I. Pritchard, and S. T. Britland, “Greenbottle (Lucilia sericata) larval secretions delivered from a prototype hydrogel wound dressing accelerate the closure of model wounds,” Biotechnology Progress, vol. 22, no. 6, pp. 1690–1696, 2006.

3) Dariusz Waniczek, Andrzej Kozowicz, Małgorzata Muc-Wierzgoń, Teresa Kokot, Elżbieta Świętochowska, and Ewa Nowakowska-Zajdel, "Adjunct Methods of the Standard Diabetic Foot Ulceration Therapy,"  Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 243568 Chapter 3

4) P. E. Prete, “Growth effects of Phaenicia sericata larval extracts on fibroblasts: mechanism for wound healing by maggot therapy,” Life Sciences, vol. 60, no. 8, pp. 505–510, 1997.

5) R. A. Sherman, "Mechanisms of Maggot-Induced Wound Healing: What Do We Know, and Where Do We Go from Here?" Evidence-Based Complementary and Alternative Medicine
Volume 2014 (2014), Article ID 592419

6) R. A. Sherman, “Maggot therapy for foot and leg wounds,” International Journal of Lower Extremity Wounds, vol. 1, no. 2, pp. 135–142, 2002.

7) R. A. Sherman, "Maggot Therapy takes us back to the future of wound care: New and Improved Maggot Therapy for 21st Century" J Diabetes Sci Technol. 2009 Mar; 3(2): 336–344.

8) U. Wollina, K. Liebold, W. Schmidt, M. Hartmann, and D. Fassler, “Biosurgery supports granulation and debridement in chronic wounds—clinical data and remittance spectroscopy measurement,” International Journal of Dermatology, vol. 41, no. 10, pp. 635–639, 2002.

9) Wikipedia, "Maggot Therapy"

10) W. Robinson, “Stimulation of healing in non-healing wounds by allantoin occurring in maggot secretions and of wide biological distribution,” Journal of Bone and Joint Surgery, vol. 17, pp. 267–271, 1935

11) Z. Zhang, S. Wang, Y. Diao, J. Zhang, and D. Lv, “Fatty acid extracts from Lucilia sericata larvae promote murine cutaneous wound healing by angiogenic activity,” Lipids in Health and Disease, vol. 9, article 24, 2010.

12) Z. Zhang, S. Wang, X. Tian, Z. Zhao, J. Zhang, and D. Lv, “A new effective scaffold to facilitate peripheral nerve regeneration: chitosan tube coated with maggot homogenate product,” Medical Hypotheses, vol. 74, no. 1, pp. 12–14, 2010.