undefined

Sometimes that is such a hard question. How do you deal with pain?

There are many of us, that suffer with pain, either in our bodies or the heartachs we deal with daily. People that dont have pain 24/7 do not understand or some cant realize how much we go though. To wake up and go to sleep (if you can sleep) at night in pain, is a horrible way to live. Some (even family, children, friends) back away from you because you are sick or in pain, or both.

Such a sad thing to me when I see others suffering, and I can relate and understand them totally. My heart just breaks, as I love to see another healthy and happy.

The way I deal with my pain daily, and I mean all the time, is to continue the joy that God gives to me, along with only His strength. If it was not for that, I would not want to live this way anymore. I know its not me, that jokes around, or can keep going on daily, it is some higher power working in and though me. Does this mean I'm not in pain..heck NO..it means I can smile, I can be a blessing to another, I can make others laugh, I can love the lost, I can try to help and let others know...that there is hope. There are many times, that I just cry out and wish God would just take me home, yes Im human too..yet I know that is not up to me, and there is some reason beyond my thinking why Im still here and why I keep pushing on.

Doctors many times, give up on you, tell you its hopeless, there is no more to do, you will suffer and get worse as your life continues. They find all this stuff wrong inside you, and its serious, and want to put you on yet another pill that makes you sick. Well shoot..isn't the pain enough that to deal with feeling sicker too? So what do we do? Well, you keep pushing on, you keep smiling, you keep praying most of all, you keep holding tight to Gods hands, you keep being a blessing, you just keep on keeping on..and when you feel like you cant any longer...you press though it..you get yourself around people that really CARE that really LOVE you the way you are. You keep that heart that cries out to be loved and understood, and keep your mind set and your heart set on knowing how blessed you are, because there is always someone worse than you are. You ask..."Really, no one can hurt as much as I do." Yes, they can, and yes there is that someone.

Is it hard? Omg sure it is..very hard.  So press on and when you feel lost, or your loved one's hurt you, or leave you alone, you press on even harder. You hold onto Gods unchanging hand..His love for you..

Go into a place, where you can be alone, and just breath, and the Lord hold you. You might ask, "Well I dont know what to say anymore, I have cried so much, I cant cry anymore." God understands that, He just understands YOU, and He hears all your hurt, and feels all your pain, though your tears. You dont have to say a word.

Im not preaching at ya..but letting you know what I do when it gets so un-bearable I CANT stand it much longer. And remember there is joy in the morning. Meaning..tomorrow just might be a better day for you, if not..there is always another tomorrow. Many say, "how much more, how much more strength do I need to keep going on in such pain and/or sorrow?" Well, when your strength and joy is just pure gone, that is when God steps in. He will give you more. He will give you that smile, to go on, press on, press though, and not Give Up!!

That smile you see on my pics, is sometimes so hard to do, remember I understand constent pain. Yet, when I smile, it does something inside me, it not only comforts me, but others, and when you are a blessing to other's, things seem better, because you are helping and encouraging someone just like you. That person might just need that, or need that smile you share, or need a hug, and it just might save them from giving up.

I love ya all, and I'm here if ya need me. You know how to find me.

Welp, Im tierd  and will say goodnight, for now with this blog, and God bless you all and remember..He "just" understands your tears.

No wheelchairs in Heaven
Life isn't always easy
Sitting in a wheelchair
Sometimes I get discouraged
And loaded down with care

That's when I lean on Jesus
To help me through the day
For he gives me peace and comfort
When trials come my way

The Bible says there is a place
That someday I will see
Where there will be no sickness
Or pain to bother me

I'll walk upon a street of gold
Glorious beauty I will share
In a place called Heaven
Where I'll need no wheelchair

The Faithful Friend

Realationships are important in life. You will need friends and friends will need you. That is why it is important to develop healthy friendships. When you build your life around a few dysfunctional relationships, you will find yourself empty and abandoned at the time when you need friends the most.

This is why it is important not to build your life around "unfaithful" friends. Realize the importance of building strong, health friendships. One characteristic that distinguishes between a healthy and unhealthy friendship is faithfulness. Is the person faithful in his/her friendship with you? Friends are important in the good times and the bad times. Unfaithful friends will be tehre for the good times, but they will abandon you in the bad times. The ultimate test of a true friend is their faithfulness to you in the hard times.

Are you a faithful friend? Faithfulness is an important characteristic for you to be developing in your life. A faithful friend is different from a codependent friend. A faithful friend's actions are based on legitimate concern for the friend, while a codependent's actions are based on a dysfunctional need for that friend. There is a subtle difference in the actions, but the motivations are very distinct.

The clinical picture associated with pathology of the autonomic nervous system

The autonomic nervous system contains three main components -

1. The Hypothalamic-Pituitary axis,
2. The Ascending pathways in the brain from the basal ganglia
3. The Descending autonomic sympathetic and parasympathetic pathways from the hypothalamus to the viscera.

Causes of peripheral autonomic dysfunction

• N utritional deficiency - Vitamin B1, 3, 6, 12
• N eurological - Multiple sclerosis, Guilliane Barre, spinal cord injury
• E ndocrine - Diabetes, Porphyria, Addisons, Growth Hormone excess
• U nknown - Idiopathic
• R enal failure
• O there! - Sarcoid
• P araneoplastic phenomena
• A utoimmune - Lupus, Rheumatoid, Sceloderma
• A bnormal Proteins - Multiple Myeloma
• T oxins and drugs - Alcohol and Ionizide
• H uman Imunodeficiency Virus
• Y Chromosome - Congenital

Symptoms, signs and treatment:

• Postural dizziness - elastic stockings, ephedrine, tyrosine, beta-blockers, mineralocorticoids e.g. Fludrocortisone 0.1-0.3mg daily.
• Reflux oesophagitis and delayed gastric emptying - metoclopramide 10mg before meals.
• Nocturnal diarrhoea - metoclopramide 10mg 8 hourly, a short course of tetracycline may be of benefit to the patient.
• Post gustatory sweating - anticholinergics - propantheline hydrobromide before meals.
• Bladder dysfunction and urinary retention - regular voiding and antibiotics for infections.
• Impotence - counseling, pharmacological erections and penile implants.
• Cardiorespiratory arrest - maintain high FiO2 at all times.
• Pupillary abnormalities
• Thermal irregularities
• Skin colour abnormalities.

Tests for autonomic dysfunction.

1. Parasympathetic Heart rate response to a Valsalva manoeuvre . A correctly preformed Valsalva manoeuvre involves forced expiration, generating a pressure of 30mmHg, against a closed glottis for 5 seconds.

   Blood pressure, as it is a gauge pressure, increases at the beginning of the manoeuvre. The baroreceptors cause a transient decrease in heart rate during this period. The raised intrathoracic pressure impedes venous return which causes a decrease in cardiac output, and the blood pressure then gradually decreases to below baseline, despite the baroreceptors causing a progressive tachycardia and peripheral vasoconstriction. On release of glottic closure, the blood pressure will drop because it is a gauge pressure, further rising the heart rate. The compensatory reflexes combined with a now unimpeded venous return to the heart will cause the blood pressure to steadily rise, most often to above baseline until all the compensatory mechanisms and the heart rate have returned to normal These dramatic variations in heart rate are absent in autonomic dysfunction

2. Heart rate variation during quite inspiration and expiration is lost with autonomic dysfunction.

   Heart rate response to standing. In order to compensate for the decrease in blood pressure from the lying to standing position there is a reflex tachycardia which is maximal after ~ 15 beats. Blood pressure is restored to above baseline which causes a reflex Brady cardia which is maximal after ~ 30 beats. Sympathetic

3. Postural hypotension.

   On standing the decreased blood pressure is usually compensated for by a reflex tachycardia and vasoconstriction, neither of these mechanism work well in autonomic dysfunction leading to a marked difference in systolic blood pressure between lying and sitting / standing. The normal is <10mmHg, pathological is when the difference is >30mmHg.

4. Blood pressure response to sustained handgrip.

   Sustained handgrip as measured by a dynamometer causes a reflex increase in heart rate and cardiac output without changing systemic vascular resistance, diastolic blood pressure thus normally increases.

Peri-operative management

Pre-operative History to elicit the cause of the neuropathy and the degree of symptomatology present. Co-morbid disease should be activly sought.

The examination is directed at finding evidence of cardiac decompensation and concommitant peripheral neuropathy.
A thorough airway evaluation is necessary.
Bed side examination for autonomic dysfunction generally involves finding postural hypotension and noting the heart rate response to a Valsalva manoeuvre.

Investigations area aimed at determining the degree of renal dysfuntion, checking the degree of myocardial ischaemi and cervical spine X rays for ligament laxity.

Premedication

• Decrease the amount of residual gastric volume - Metoclopramide 0.1mg/kg
• Increase the pH of the residual gastric volume - Ranitidine 2mg/kg nocte and mane orally combined with 0.3Molar sodium citrate, 30mls orally immediately prior to induction

Intra-operative Anaesthesia technique

Induction
Good pre-oxygenation followed by a rapid sequence intubation with a cuffed oral tracheal tube.
If a difficult larygoscopic view is anticipated then endotracheal intubation must be secured while the patient is awake
Centroneuraxial naesthesia is complicated by difficult blood pressure maintenance.
The presence of peripheral neuropathy must be well documented prior to any regional procedure

Maintenance
Inhalational anaesthesia with air, oxygen and a volatile agent titrated to effect Opioid supplementation must be done judiciously to avoid precipitate drops in blood pressure and post operative respiratory depression

Emergence
Complete reversal of any non-depolarising muscle relaxant to ensure excellent airway control. Extubate the patient only when fully awake and in the recovery position with good suction available.

Monitoring

• ECG for ischaemia and rhythm abnormalities.
• Arterial line pre-induction and connected throughout positioning of patient for beat to beat variations of blood pressure, with quick aggresive correction of hypotension - Phenylephrine 50 mg boluses, followed by an infusion of 0.15 to 1 mg/kg/min
• Central venous pressure and urine output for optimal fluid balance
• Temperature probe.

Positioning and padding
Slow controlled positioning is necessary to avoid sudden blood pressure changes.
These patients are at an increased risk of iatrogenic nerve injuries so excellent attention must be paid to padding vulnerable areas

Post operative
Supplemental oxygen (40%) and close respiratory monitoring for at least 24 hrs.
Close haemodynamic monitoring, with correction of hypotension for at least 24 hours
Good post operative analgesia - patient controlled analgesia or regional anaesthesia or nurse controlled, with anti-emetic prophylaxis 

Powered by

English

Albanian

Arabic

Bulgarian

Catalan

Chinese

Croatian

Czech

Danish

Dutch

Estonian

Filipino

Finnish

French

Galician

German

Greek

Hebrew

Hindi

Hungarian

Indonesian

Italian

Japanese

Korean

Latvian

Lithuanian

Maltese

Norwegian

Polish

Portuguese

Romanian

Russian

Serbian

Slovak

Slovenian

Spanish

Swedish

Thai

Turkish

Ukrainian

Vietnamese

HI EVERYONE. I HAVE ARACHNOIDITIS, ALONG WITH OTHER THINGS TOO, BUT I WANTED TO LET YOU KNOW THAT THERE IS STILL HOPE FOR ANY OF YOU THAT MIGHT HAVE THIS OR ANYONE THAT IS SUFFERING IN ANY OTHER KIND OF PAIN. PLEASE DONT GIVE UP. READ MY BLOGS, AND BE TOUCHED BY MY MAIN PAGE ON MYSPACE. THE LORD PLACED IT IN MY HEART TO GET THIS WORD OUT CONCERNING THIS PAINFUL, HORRIBLE DESEASE THAT HAS NO CURE. BUT LET ME TELL YOU, THE LORD WILL HELP YOU, EASE THE PAIN, CAN EVEN HEAL YOU, IF YOU ALLOW HIM TOO. HE IS THE ONLY ONE THAT GIVES ME PEACE, AND HAPPINESS, LOVE AND THE SMILE YOU SEE ON MY FACE THOUGH IT ALL, AND THOUGH THE PAIN I SUFFER IN 24/7. AND BELIEVE ME, ITS HORRIBLE PAIN. I WILL LET YOU READ WHAT ARACHNOIDITIS IS BELOW. AND IF YOU NEED TO TALK, PLEASE FEEL FREE TO MESSAGE ME AND I WILL GET BACK TO YOU. GOD BLESS YOU ALL, AND HANG ON, THERE IS HOPE FOR YOU!! IF THERE IS FOR ME, THERE IS FOR YOU TOO!

..TR>

..TABLE>

ORIGIN The usual causes of spinal arachnoiditis are 1.       Infections like tuberculosis, AIDS, fungus       (cysticercosis) and meningococcus, etc. 2.       Dyes used for myelograms like pantopaque, metrizamide, omnipaque, etc. 3.      Blood entering the spinal sac, I.e. From subarachnoid hemorrhage, epidural blood patches, bleeding from anticoagulants, etc. 4.      Spinal surgery, mostly from rents (recognized or unrecognized) of the dura with blood entering the sac (this is the most common cause today), direct SC or nerve root injury. 5.      Irritant compounds injected into the sac such as hypertonic saline, phenol, methotrexate, hyaluronidase, papain, etc. 6.      Preservatives contained in some medications injected into the spine such as polyethylene glycol, benzylic alcohol, para-aminobenzoic acid, etc. 7.      Traumatic injury to the SC or the brain may result in bleeding into the CSF, nerve tissue damage or avulsion. Even needle punctures causing paresthesia on the nerve roots or the SC (from peridural, spinal anesthesia or other nerve blocks) may cause ARC.

TOPOGRAPHY Cerebral ARC may occur in the optic chiasm (usually from sinus infection) and in the lateral and posterior fossae of the skull (from chronic ear infections or parasites). Spinal ARC may appear as localized when it is at one intervertebral level; diffuse as from infiltrating tumors of the spine; distant when subarachnoid hemorrhage in the brain may result in spinal ARC; segmental when it is present in two or more separate levels; and contiguous if it includes two or more adjacent vertebral levels of the spine. Cauda equinoid and cauda equina syndromes are mild and moderate lesions located on the distal point of the SC are truly varieties of ARC, as well as syrinx (loss of most of the normal pattern and mapping of the SC), syringomyelia representing cavitary lesions, and pseudomeningocele consisting of secondary, thin, false sacs adhered to or behind the dura (usually containing some nerve roots)—all are different presentations of ARC.

..TR>

..TABLE>

PATHOLOGICAL PROCESSES This is indeed a complex illness because in the majority of these patients, ARC occurs as an iatrogenic complication from either a diagnostic (myelogram) or a therapeutic (laminectomy) procedure. So, both the symptoms and the radiological findings are superimposed to the patient's disease that motivated the intervention, making a specific profile for ARC difficult to define, if not impossible. Immediately after the injurious event, an acute inflammation takes place next to and adjacent to the site of entry, depending on the extent and volume of irritant in relation to the volume of the CSF and hydration of the patient. Depending on the location, radiculitis may be the earliest manifestation, with swelling of the nerve roots that became in greater contact with the offending agent. Swelling of the adjacent arachnoid creates acute arachnoiditis with increased vascularity, venous congestion, and hyperemia. This inflammatory phase either progresses and becomes more severe and more extensive (especially if repeated insults occur and/or the patient's immune system hyperreacts) or it may gradually subside, especially if anti-inflammatory (steroid and non-steroid) agents are administered. After an interval of 4 to 7 months, the syndrome may move into a proliferative phase when collagen and fibroblasts appear, gradually forming adhesions, fibrosis and scarring which make nerve roots adhere to each other and to the meningeal sac, which may also be deformed in a constrictive manner (obliterative arachnoiditis) to the point of obstructing the DS, partially interfering with the normal flow of CSF, or obliterating it completely as in pachymeningitis.

DYSFUNCTIONAL EVENTS Throughout these processes, the affected nerve roots generate exaggerated electrical impulses to the dorsal horn of the SC, where a complex system of receptors, inhibiting pain pathways, and neuron connections are located. These exaggerated impulses eventually make the receptors oversensitive, and may interfere with inhibitory relays to the point that pain is perceived to be of greater and greater intensity, which creates a self-feeding mechanism, expands to adjacent areas, and appears to increase in intensity ("wind-up" phenomenon and distribution). It may also produce severe muscle spasms when ventral roots are affected. There is evidence that the sympathetic nervous system is affected, represented by sweating, heat intolerance, trophic changes, night sweats, low-grade fever, etc. MANIFESTATIONS The symptoms vary, but pain is the predominant complaint—most frequently burning sensations (92%), throbbing and sharp pains on the lower back, legs and feet. Numbness and tingling sensations are frequent, while atypical headaches, blurred vision and insomnia seem to be systemic manifestations. Bladder dysfunction is prevalent mainly in women (incontinence).  Rectal dysfunction is less common, but sexual (organic and emotional) dysfunction is more prevalent. Psychological manifestations are frequently seen in patients with chronic pain; in patients with ARC, depression is common in about 80% of them secondary to despair, hopelessness, fear of income loss, and/or family disputes, in some cases leading to thoughts of self-injury.

..TR>
..P>

5:14 PM 

0 Comments

(Add Comment) |

0 Kudos

Translate

RADIOLOGICAL DIAGNOSIS Current technology allows for prompt and precise diagnosis of the characteristic lesions of ARC; specifically, MRI defines the location and the extent of intraspinal (intra and extradural) pathology. Thickened and swollen nerve roots and cauda equina can be identified as early as one or two days after the injurious event. Clumped nerve roots may not be seen until months later, indicating a maldistribution of the usually orderly mapping of the roots located at the most dependent portion of the dural sac, surrounded by and floating in CSF at the lumbar region. In worse cases, deformities of the dural sac, adherence of the roots to the sac wall, fibrosis and scarring may appear. CAT scans may show skeletal, ligament and muscle abnormalities, and extradural intraspinal lesions, but only when it is preceded by myelography would intradural structures be recognized (except calcifications). The author is against the risk of unnecessary myelograms, but when metal hardware is present, since the diagnosis is crucial, this method may have to be used, as long as water-based dyes are injected. It is acknowledged that this type of contrast media may also produce ARC. The expertise of the radiologist interpreting the films is imperative to achieve a precise diagnosis of ARC, and adequate hydration of the patients will ensure reduced concentration of the dye used. TREATMENT Unfortunately, there is no cure for arachnoiditis. In the acute inflammatory phase of ARC, the administration of systemic and intraspinal corticosteroids may prevent the evolution into the chronic phase. Pain may be treated with indomethacin, dipyrone or ibuprofen; in addition, d-penicillamine and colchicine are helpful.  Oxybutynin usually improves urinary incontinence, and sildenafil citrate has been shown to correct most cases of impotence; however, the alterations of sexual function are much more complicated, with loss of libido and especially low back and lower extremity pain during and after intercourse. Muscle relaxants are indicated if muscle spasms are severe and not susceptible to treatment with physical therapy and reconditioning. Once the proliferative phase starts, any intervention may exacerbate the pain path mechanisms; therefore, invasive procedures have to be selected if the risk/benefit ratio is favorable. Epidural steroids are helpful in producing temporary pain relief and reducing the extradural formation of fibrosis; so is the epidural and intrathecal infusion of analgesics. SC stimulation reduces pain temporarily in localized (mononeuronal) cases. Neuroplasty is contraindicated because it requires the injection of 10% hypertonic saline and hyaluronidase that produces arachnoiditis. The surgical breakdown of adhesions, even when performed meticulously under the microscope carries a great risk because SC dysfunction may be aggravated; laminectomies, foraminotomies and spinal fusions would need to be absolutely indicated because of the potential danger of recurrent dural sac injury and entry of blood. Long-term opioid therapy is not to be taken lightly, especially with Schedule II "slow-release" preparations; the consequences of drug dependency are intangible, but very real, with serious behavioral alterations.  Medications in Schedule III are preferred. A variety of new therapeutic agents and interventional modalities are being proposed mostly for the symptomatic treatment of ARC; however, the most important therapy is prevention, since most of these cases are iatrogenically caused.  Education of physicians, nurses, and technicians regarding the numerous causes of this disease is an essential initial step, followed by the information to the public in general, and to patients with spinal disease in particular, so as to warn them against accepting questionably effective procedures in desperation to have their pain relieved and to procure competent and responsible physicians in their care.  Once an injurious event takes place, prompt action to define the precise diagnosis and to institute treatment is primordial. There is no place for hesitation since there is only a short window of opportunity during which chances to reverse the process are feasible. Once the proliferative phase begins, there is only symptomatic treatment.

Powered by

English

Albanian

Arabic

Bulgarian

Catalan

Chinese

Croatian

Czech

Danish

Dutch

Estonian

Filipino

Finnish

French

Galician

German

Greek

Hebrew

Hindi

Hungarian

Indonesian

Italian

Japanese

Korean

Latvian

Lithuanian

Maltese

Norwegian

Polish

Portuguese

Romanian

Russian

Serbian

Slovak

Slovenian

Spanish

Swedish

Thai

Turkish

Ukrainian

Vietnamese