PROTEIN REQUIREMENTS

 Tube Feedings: Enteral Nutrition

1. Indications for Enteral Nutrition: the preferred route - "If the gut works, use it"

• Mechanical GI tract dysfunction/disorders - may have normal digestive & absorptive function with an oral/mechanical/physiological obstruction
• Facial/jaw injuries, head & neck CA, swallowing disorders, obstruction of the upper GI tract, GI tract fistulas, short bowel syndrome (feed beyond the obstruction/fistula)
• Metabolic GI tract dysfunction - may have impaired ability to digest & absorb nutrients
• Pancreatitis, infalmmatory bowel disease, radiation enteritis, chemotherapy
• Hypermetabolic conditions - may have increased energy & protein requirements that cannot be met with regular oral intake
• Major burns, trauma, sepsis, post-operative recovery following surgery

2. Contraindication for Enteral Therapy: GI tract not working

• Intractable vomiting
• Intestinal obstruction
• Upper GI tract hemorrhaging
• Severe, intractable diarrhea
• Severe, acute pancreatitis
• Expected need less than 5-10 days

3. Routes:

Short-term: Nasogastric, Nasoduodenal, Nasojejunal Long-term: Gastrostomy & Jejunostomy (surgically placed) and PEG - percutaneous-esophago-gastrostomy & PEJ - percutaneous-esophago-jejunostomy (endoscopically placed)

4. Tubes

Tube size: Consider viscosity of formula; select the smallest appropriate size for patient comfort. 8 French can generally be used for commercial formulas while the patient will need a 10-14 French for blenderized formulas.
Tube length: Depends on tube placement, with a 30" length for nasogastric feeding and 43" for nasoduodenal & nasojejunal feedings.

5. Selecting the formula: based on patient need

Consider each of the following factors:

• How well the GI tract is functioning and its capacity
• Underlying disease conditions
• Patient tolerance

Enteral Formula Categories

Category	Subcategory	Characteristics	Indications
Polymeric	Standard	Similar to average diet	Normal digestion
	High nitrogen	Protein>15% of total kcal	Catabolism Wound healing
	Caloric dense	2 kcal/ml	Fluid restriction Volume intolerance Electrolyte imbalance
	Fiber containing	Fiber 5-15 g/L	Regulation of bowel function
Monomeric	Partially hydrolyzed	One or more nutrients are hydrolyzed. Composition varies.	Impaired digestive and absorptive capacity
	Elemental
	Peptide based
Disease- Specific	Renal	Less protein, low electrolyte content	Renal failure
	Hepatic	High branched chain amino acids (valine, isoleucine and leucine, which are known as the stress amino acids), low aromatic amino acids (phenylalanine; tyrosine; tryptophan), low electrolyte content	Hepatic encephalopathy
	Pulmonary	Higher % of calories from fat instead of carbohydrates	ARDS
	Diabetic	Low carbohydrates	Diabetes mellitus
	Immune-enhancing	Arginine, glutamine, omega-3 fatty acid, antioxidants	Metabolic stress Immune dysfunction

from http://www.rxkinetics.com/tpntutorial/2_1.html (Note: N170 students responsible for Nutritional concepts and Enteral Nutrition ONLY)

6. Administration of feedings

• Bolus
• Intermittent
• Continuous

	Indications	Advantages	Disadvantages
Bolus	Noncritically ill patient Home TF Rehabilitation patient	Easy to administer Inexpensive Short administration time (usually 15 minutes)	Highest risk of aspiration, N/V, abdominal pain and distention, and diarrhea
Intermittent	Noncritically ill patient Home TF Rehabilitation patient	Flexibility in feeding schedule Inexpensive Feeding over shorter time allows patient more free time	Higher risk of aspiration, N/V, abdominal pain and distention, and diarrhea May require formula with more calories and protein
Continuous	Initiation of tube feedings Critically ill patient Small bowel feeding Intolerance of intermittent or bolus	Pump assisted Minimizes risk of high gastric residuals and aspiration Minimizes risk of metabolic abnormalities	Restricts ambulation Infused over 24 hours/day Increased cost (need pump)

7. Feedings started:

• In the past tube feedings that were hyperosmolar were diluted ½ strength - current recommendations are to leave the formula full strength and begin at a lower volume until tolerance is determined.
• Full strength if isotonic - DO NOT DILUTE ISOTONIC FORMULAS!
• Tube feeding is progressed until assessed nutrition goal reached
• If TF is diluted, do not advance concentration and rate at the same time

8. Tolerance

• Check gastric residuals
• Diarrhea
• Constipation
• Bloating and excess gas production

9. Sanitation

• bag and tubing is changed every 24 hours, but check your hospital protocol
• formula is administered at room temperature

TF should not be started until an X-ray shows the tube is in the proper place, then formula can be started
Head of bed (HOB) must be elevated at least 30° at all times.

Epidemiology of Complex Regional Pain Syndrome: A Retrospective Chart Review of 150 Korean Patients

J Korean Med Sci. 2008 October; 23(5): 772–775.

Published online 2008 October 30. doi:  10.3346/jkms.2008.23.5.772

PMCID: PMC2580014

Epidemiology of Complex Regional Pain Syndrome: A Retrospective Chart Review of 150 Korean Patients

Yun Suk Choi,^* Mi Geum Lee,^† Hyo Min Lee,^‡ Chul Joong Lee,^§ Ji Yeon Jo, Soo Young Jeon, Sang Chul Lee, and Yong Chul Kim

Author information ► Article notes ► Copyright and License information ►

This article has been cited by other articles in PMC.

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Abstract

Complex regional pain syndrome (CRPS) is a chronically painful and disabling disorder. However, no data are available even on the epidemiology of CRPS in Korea. This study was undertaken to retrospectively assess the epidemiologic characteristics of CRPS in 150 consecutive patients at a tertiary chronic pain center from March 2002 to February 2006. Information was obtained regarding patients' demographics, nature of injury, and treatment modalities. Seventy-one percent of patients had CRPS type I. The mean 11-point verbal numerical rating scale score at initial examinations and at the time of study were 8.0 and 5.7, respectively. Thirty-two percent of patients showed no change or increase in pain intensity during follow-up at our pain center. The mean duration of CRPS symptoms prior to our pain center evaluation and prior to the time of study were 27 months and 50 months, respectively. These patients had seen on average 5 different physicians before being referred to our center. This study shows that the majority of CRPS patients were referred to our center after more than 2 yr of symptoms. The clinical implication of such delayed transfer and strategies to avoid this problem are discussed.

Keywords: Complex Regional Pain Syndromes, Epidemiology, Treatment

INTRODUCTION

Complex regional pain syndrome (CRPS) is associated with topical pain, which develops primarily after trauma. The intensity and duration of CRPS are highly variable, though CRPS can induce serious impairment of the autonomic nervous system and of motor function, and consequently can result in diverse clinical outcomes.

The development of CRPS may be explained by various mechanisms, such as alterations in the central nervous system or by biofeedback from the sympathetic nervous system, but the underlying mechanism remains to be clarified. Although definite measures for the diagnosis and treatment of CRPS are being actively pursued (1, 2), as yet no objective diagnostic criterion nor a simple reliable test has been established. For this reason, it usually takes a long time to the final diagnosis of CRPS, which ultimately renders treatment outcomes worsened. Moreover, in Korea, not even epidemiological studies have been conducted as yet. Therefore, the aim of this study was to assess the epidemiologic characteristics of CRPS for the first time in Korean patients.

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MATERIALS AND METHODS

This retrospective study was approved by our institutional review board. The medical records of 150 consecutive patients diagnosed with CRPS at our pain center from March 2002 to February 2006 were reviewed and current patient status was determined using telephone interviews. At initial visits, all available prior medical data including neurological and radiological data were reviewed. 

Twenty-three patients were lost to follow-up and 7 had died, and thus, 120 patients were interviewed by telephone. Present pain intensity and the treatment modality regarded to be most helpful for alleviating pain were recorded. For each finding, patient percentages were calculated based on a responder basis rather than on total patient number.

Diagnoses were made in our pain center using the modified International Association of the Study of Pain (IASP) diagnostic criteria for CRPS (3). Many ancillary tests, such as, neuromuscular conduction, quantitative sensory, and autonomic function tests (including diagnostic sympathetic block), and infrared thermography and a 3-phase bone scan were usually performed at initial visits and during follow-up. Infrared thermographic results were interpreted as positive when the temperature difference between ipsilateral and contralateral extremities was ≥0.6℃ (4). Results of 3-phase bone scans were interpreted as positive when a difference in early blood pooling with or without an increase in diffuse bony uptake was observed (5).

The following details were available for analysis: patients' age, gender, type of CRPS, site of lesion, injury profile, pain intensities at presentation and at the time of study, duration of CRPS symptoms prior to our pain center evaluation and prior to the study, the number of physicians who had treated patients before referral to our center and their medical fields, the treatment modalities received, the treatment modality considered by patients to be most effective, and the presence of a history of spinal cord stimulation (SCS). Pain intensity was rated using an 11-point of verbal numerical rating scale (VNRS).

Data are presented as means±SD. Statistical analyses were performed using descriptive statistics.

RESULTS

Eighty-three patients (55%) were male and 67 (45%) were female (0.8: 1 female-to-male ratio). Patients' mean age at initial evaluations was 45±14 yr, and mean age at time of injury was 40±45 yr and 43±19 yr for male and female patients, respectively. CRPS developed most frequently in the third decade (22 patients) and in the fifth (22 patients) in men. The military personnel was 73% (16 patients) in the third decade. In female patients, CRPS developed most frequently in the fifth decade (18 patients), followed by the forth (16 patients) and sixth (13 patients) (Fig. 1). Seventy-one percent of patients had CRPS type.

Fig. 1

Distribution of cases by age and sex.

Mean VNRS scores at initial evaluations and by telephone interview were 8.0±1.9 and 5.7±2.5, respectively. Thirty-eight patients (32%) showed no change or increase in pain intensity during follow-up treatment. The mean durations of CRPS symptoms prior to our initial pain center evaluation and prior to the time of study were 27±52 months and 50±53 months, respectively, and 5±5 (range, 0-40) physicians were visited before referral to our center. Crush injury, surgery, and fall down trauma were common causes of CRPS (68 patients, 45%) (Fig. 2). Eighty-two percent of the patients complained of pain in one extremity only, and lower extremities (55%) were more commonly affected than upper extremities (27%). Eighteen percent complained of a pain in the face or chest. Seventy-five percent of patients had been treated by ≥1 anesthesiologist before being referred to our pain center.

Fig. 2

Types of injuries precipitating the development of CRPS.

The treatment modalities which were used at our pain center included physical therapy, pharmacotherapy, sympathetic blocks and/or chemical neurolysis, radiofrequency lesioning, intravenous infusion of ketamine or lidocaine, intravenous regional block, and spinal cord stimulation. Pharmacotherapy was the most common form of therapy (91 patients), followed by sympathetic block (42 patients), intravenous infusion of ketamine (36 patients), and/or nerve blocks (35 patients) (Fig. 3).

Fig. 3

 

The number of patients for each of the treatment modalities.

Seventy-six percent reported that sympathetic block or neurolysis including radiofrequency lesioning was the most effective treatment. Twenty-three percent of patients (24/108 patients) were implanted with a spinal cord stimulator (SCS). However, 38% (9/24) had their SCS removed during follow-up, but on the other hand, 21% (5/24) responded that they considered SCS stimulation the most effective treatment modality (Fig. 4). One patient received dorsal rhizotomy and a limb amputation, and 1 patient committed suicide.

Fig. 4

 

The percent of patients who reported this treatment most effective.

DISCUSSION

Little published data are available on the epidemiology of CRPS, and this study is the first epidemiologic study of CRPS that was conducted in Korea. Overall, the epidemiologic data collected during this study are similar to those of previous studies (6, 7). However, our data showed a female-to-male ratio of 0.8:1, which does not concur with the findings of other studies, which have found that CRPS more commonly develops in women at gender ratios of 1:2.3-1:4.5 (6, 8, 9). In the present study, the condition occurred more often in male patients aged 20-29 yr than in other age groups. Obligatory military service in Korea may have increased the risk of trauma in this age group. The mean duration of CRPS symptoms prior to presentation at our pain center was 27 months, which is similar to that found by Allen et al. (6), but longer than that reported by Sandroni et al. (7). It is known that a prior injury, e.g., fractures, contusions, sprains, and surgical traumas, is the main cause of CRPS (6). The present study also shows that injuries such as traffic accidents and falls are leading causes of CRPS and that surgical trauma contributed to a lesser extent, which concurs with that reported elsewhere (6, 7). In addition, in the present study, immobilization due to a splint, gun shot wounds, tooth extractions, injections, and pregnancies were all found to induce CRPS.

We found that a lower limb was affected approximately twice as often as an upper limb, which concurs with the findings of Allen et al. (6). However, Sandroni et al.(7) reported that CRPS developed more frequently in an upper limb than in a lower limb. Moreover, in this study (7) bilateral side involvement was observed in some cases as an early manifestation. The over-expression of symptoms in relation to the reward may in part explain this phenomenon.

In the present study, the type I: type II ratio was 7:3, which differs from that reported by a previous study which indicated that the incidence of CRPS type II was extremely rare except during a war (10).

In the present study, pharmacotherapy was adopted most frequently, followed by a sympathetic nerve block, the intravenous infusion of ketamine, and a spinal nerve block. According to patients' subjective reports on treatment efficacy, a sympathetic block and the intravenous infusion of ketamine were the most effective treatment modalities among those treatment modalities received. Sympathetic nerve block has been reported to be only effective at treating sympathetic maintained pain, although it has been described as a first choice therapy (11). In addition, it has been reported that sympathetic nerve block is also effective at ameliorating elevated skin temperatures, edema, or allodynia that develops within 6 months (11). The present study revealed that intravenous ketamine (an NMDA receptor antagonist) was clinically effective in 44% of patients. Correll et al. (12) reported that 76% of patients with CRPS who did not respond to conventional treatment achieved complete remission after intravenous ketamine administration and that 18% achieved partial remission. Moreover, they found that the therapeutic effects of intravenous ketamine lasted between 3 and 12 months and that it could be reperformed in recurrente cases, although it was also found on occasions to induce headaches and hallucinations. SCS reduces the pain via neuromodulation. Taylor et al. (13) concluded that SCS is effective in 70% of CRPS patients and more cost-effective than conventional treatments. In our previous report (14), 57% of CRPS patients rated SCS as having an excellent or good effect. In this present study, 23% of patients underwent SCS implantation, but 62% of them have been used SCS at the time of study and only 20% of them was the most effective treatment modality they had encountered. Based on the present study, the possible reasons for the high removal rate and relatively low satisfaction with SCS were delayed diagnosis and treatment, high initial cost, higher dosage of opioids, high initial pain score, inaccurate evaluation of the effect of trial stimulation, and too high expectation of the benefits of SCS. After covering the cost of SCS by the National Health Insurance System in Korea on August 1 2005, the incidence of SCS implantation has increased year on year, and this might well increase future satisfaction rates.

At initial examinations, the mean VNRS score of patients was 8.0, which is similar to that reported previously (15). The mean VNRS score reduced to 5.8 after treatment, but 32% of patients showed no change or further symptom aggravation. 

Although a considerable number of patients with CRPS experience spontaneous remission (7), CRPS became an intractable chronic pain in one third of our cases, and some of these required dorsal rhizotomy or limb amputation. CRPS is more successfully treated when patients are early diagnosed and treated aggressively, as the risk of intractable chronic pain increases as the time between symptom onset and final diagnosis increases (16). In the present study, treatment outcomes were thought to be poorer than in a previous study (7) because the time between onset and final diagnosis of CRPS was longer. This poorer treatment outcome may also be attributed to the fact that patients in the present study had relatively severe pain and a long illness duration. Therefore, we advise that patients suspected of having CRPS be referred to specialists or specialty clinics to ensure early diagnosis and treatment.

This study had some limitations. First, it was intrinsically limited by its retrospective nature. Second, some cases were lost to follow-up and finally, the study subjects analyzed were treated at one university-based tertiary chronic pain center.

In conclusion, the present study describes the epidemiologic characteristics of CRPS patients for the first time in Korea. However, the information gained is limited in terms of its general applicability to all Korean CRPS patients. Thus, we recommend that a nationwide study be undertaken with a view toward documenting the epidemiologic characteristics of Korean CRPS patients as a means of facilitating early diagnosis and treatment.

Go to:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2580014/

References

1. Kim YC. Complex regional pain syndrome. Korean J Pain. 2004;17:S104–S108.

2. Rho RH, Brewer RP, Lamer TJ, Wilson PR. Complex regional pain syndrome. Mayo Clin Proc. 2002;77:174–180. [PubMed]

3. Bruehl S, Harden RN. An empirical approach to modifying IASP diagnostic for CRPS. In: Harden RN, Baron R, Janig W, editors. Complex regional pain syndrome. Seattle: IASP press; 2001. pp. 303–313.

4. Bruehl S, Lubenow TR, Nath H, Ivankovich O. Validation of thermography in the diagnosis of reflex sympathetic dystrophy. Clin J Pain. 1996;12:316–325. [PubMed]

5. Park SH, Lee PB, Lim YH, Lee SY, Choi IY, Lee SJ, Oh YS. The usefulness of three-phase bone scan and thermography for making the diagnosis of CRPS-I. Korean J Pain. 2006;19:81–86.

6. Allen G, Galer BS, Schwartz L. Epidemiology of complex regional pain syndrome: a retrospective chart review of 134 patients. Pain. 1999;80:539–544. [PubMed]

7. Sandroni P, Benrud-Larson LM, McClelland RL, Low PA. Complex regional pain syndrome type I: incidence and prevalence in Olmsted county, a population-based study. Pain. 2003;103:199–207. [PubMed]

8. Schwartzman RJ, Kerrigan J. The movement disorder of reflex sympathetic dystrophy. Neurology. 1990;40:57–61. [PubMed]

9. Veldman PH, Reynen HM, Arntz IE, Goris RJ. Signs and symptoms of reflex sympathetic dystrophy: prospective study of 829 patients. Lancet. 1993;342:1012–1016. [PubMed]

10. Hassantash SA, Afrakhteh M, Maier RV. Causalgia: a meta-analysis of the literature. Arch Surg. 2003;138:1226–1231. [PubMed]

11. Galer BS, Schwartz L, Aller R. Complex regional pain syndromestype I: reflex sympathetic dystrophy, and type II: causalgia. In: Loeser JD, Butler SH, Chapman CR, Turk DC, editors. Bonica's Management of Pain. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001. pp. 404–408.

12. Correll GE, Maleki J, Gracely EJ, Muir JJ, Harbut RE. Subanesthetic ketamine infusion theraphy: a retrospective analysis of a novel therapeutic approach to complex regional pain syndrome. Pain Med. 2004;5:263–275. [PubMed]

13. Taylor RS, Van Buyten JP, Buchser E. Spinal cord stimulation for complex regional pain syndrome: a systematic review of the clinical and cost-effectiveness literature and assessment of prognostic factors. Eur J Pain. 2006;10:91–101. [PubMed]

14. Lee CJ, Kim YC, Shin JH, Yoo SY, Shin HY, Kim YH, Han SS, Joh JY, Lee EH, Lee SC, Park JH. Spinal Cord Stimulation in management of intractable chronic pain: a 5-year experience. Korean J Anesthesiol. 2006;51:195–200.

15. Forouzanfar T, Weber WE, Kemler M, van Kleef M. What is a meaningful pain reduction in patients with complex regional pain syndrome type 1? Clin J Pain. 2003;19:281–285. [PubMed]

16. Wakasugi B. Pain clinic shindan chiryou guide. Nilon Iji Shimosha; 1994. pp. 43–49.

Wow! That look like a nice place

Scleroderma-How Medical Marijuana Can Help Symptoms

Published by Jan

Scleroderma-


                                                                                                                                                                                                        
Scleroderma is an autoimmune disease of the connective tissue featuring skin thickening, spontaneous scarring, blood vessel disease, varying degrees of inflammation, associated with an overactive immune system.  Autoimmune diseases are illnesses that occur when the body's tissues are attacked by its own immune system.  The formation of scar tissue (fibrosis) in the skin and organs of the body characterize scleroderma.  This leads to thickness and firmness of involved areas.  Scleroderma, when it is diffuse or widespread over the body, is also referred to as systemic sclerosis.

The cause of scleroderma is unknown.  Researchers have found some evidence that certain genes are important factors, but the environment also seems to play a role.  The result is activation of the immune system in a susceptible individual, causing injury to tissues that result in injury similar to scar-tissue formation.  The fact that genes seem to cause a predisposition to developing scleroderma means that inheritance at least plays a partial role.  It is not uncommon to find other autoimmune diseases in families of scleroderma patients.  Some evidence for the role genes may play in leading to the development of scleroderma comes from the study of Choctaw Native Americans who are the group with the highest reported prevalence of the disease.  The disease is more frequent in females than in males.
Scleroderma is a chronic systemic autoimmune disease (primarily of the skin) characterized by fibrosis (or hardening), vascular alterations, and autoantibodies.  There are two major forms:
 
Limited systemic sclerosis/scleroderma involves cutaneous manifestations that mainly affect the hands, arms and face.  Previously called CREST syndrome in reference to the following complications: Calcinosis, Reynaud’s phenomenon, Esophageal dysfunction, Sclerodactyly, and Telangiectasias.  Additionally, pulmonary arterial hypertension may occur in up to one third of patients and is the most serious complication for this form of scleroderma.
 
Diffuse systemic sclerosis/scleroderma is rapidly progressing and affects a large area of the skin and one or more internal organs, frequently the kidneys, esophagus, heart and lungs.  This form of scleroderma can be quite disabling.  There are no treatments for scleroderma itself, but individual organ system complications are treated.accordinglly.  Other forms of scleroderma include systemic  scleroderma, which lacks skin changes, but has systemic manifestations, and two localized forms that affect the skin, but not the internal organs:   morphea, and linear scleroderma.
 
The cause is unknown.  Scleroderma runs in families, but the genes have not been identified.  It affects the small blood vessels (arterioles) in all organs.  First, the endothelial cells of the arteriole die off, along with smooth muscle cells, by a process of apoptosis.  They are replaced by collagen and other fibrous material.  Inflammatory cells, particularly CD4+ helper T cells, infiltrate the arteriole, and cause further damage.  Many of the inflammatory and destructive protein signals have been identified, and they are potential targets for drugs that could interrupt the process.

Individuals with morphea or limited scleroderma have a relatively positive outlook.  They will usually die from another disease, not the scleroderma.  Those with very widespread skin and organ involvement (systemic) have a negative prognosis.  More women have scleroderma, but the disease kills more men.  Following diagnosis, two-thirds of patients live at least 11 years.  The higher the patient's age at diagnosis, the more likely they are to die from the disease.  People with scleroderma have very different life expectancies.  For example, those with limited or mild diffuse disease—can expect to live 20 to 50 years after diagnosis, just like anyone else.  Others with severe, rapidly progressive disease—a group which makes up less than 10% of the total number of patients with diffuse scleroderma—might have a 50% chance of a five-year survival.
 
Symptoms

Some types of scleroderma affect only the skin, while others affect the whole body.

• Localized scleroderma usually affects only the skin on the hands and face.  It develops slowly, and rarely, if ever, spreads throughout the body or causes serious complications.

• Systemic scleroderma, or sclerosis, may affect large areas of skin and organs such as the heart, lungs, or kidneys.  There are two main types of systemic scleroderma: Limited disease (CREST syndrome) and diffuse disease.
 
Skin symptoms of scleroderma may include:

• Fingers or toes that turn blue or white in response to hot and cold temperatures)(Reynaud’s)
• Hair loss
• Skin hardness
• Skin that is abnormally dark or light
• Skin thickening, stiffness, and tightness of fingers, hands, and forearm
• Small white lumps beneath the skin, sometimes oozing a white substance that looks like toothpaste
• Sores (ulcers) on the fingertips or toes
• Tight and mask-like skin on the face
 
Bone and muscle symptoms may include:

• Joint pain
• Numbness and pain in the feet
• Pain, stiffness, and swelling of fingers and joints
• Wrist pain
 
Breathing problems may result from scarring in the lungs and can include:

• Dry cough
• Shortness of breath
• Wheezing
 
Digestive tract problems may include:

• Bloating after meals
• Constipation
• Diarrhea
• Difficulty swallowing
• Esophageal reflux or heartburn
• Problems controlling stools (fecal incontinence)
 
Treatment

There is no specific treatment for scleroderma.
Your doctor will prescribe medicines and other treatments to control your symptoms and prevent complications.

Medicines used to treat scleroderma include:
• Power anti-inflammatory medicines called corticosteroids
• Immune-suppressing medications such as methotrexate and Cytoxan
• Nonsteroidal anti-inflammatory drugs (NSAIDs)

Other treatments for specific symptoms may include:
• Medicines for heartburn or swallowing problems
• Blood pressure medications (particularly ACE inhibitors) for high blood pressure or kidney problems
• Light therapy to relieve skin thickening
• Medicines to improve breathing
• Medications to treat Reynaud’s phenomenon
Treatment usually also involves physical therapy.
 
Expectations (prognosis)

Some people with scleroderma have symptoms that develop quickly over the first few years and continue to get worse.  However, in most patients, the disease slowly gets worse.

People who only have skin symptoms have a better outlook.  Widespread (systemic) scleroderma can damage the heart, kidney, lungs, or GI tract, which may cause death.

Lung problems are the most common cause of death in patients with scleroderma.
 
Complications

The most common cause of death in people with scleroderma is scarring of the lungs, called pulmonary fibrosis.
 
Other complications of scleroderma include:
• Cancer
• Heart failure
• High blood pressure in the lungs (pulmonary hypertension)
• Kidney failure
• Problems absorbing nutrients from food (malabsorption)
 
Prevention
There is no known prevention.  Reducing your exposure to silica dust and polyvinyl chloride may lower your risk for this disease.
Because scleroderma is an autoimmune disease, one of the major pillars of treatment involves the use of immunosuppressive agents.

How Medical Marijuana (Cannabinoids) Can Help Symptoms
? Anti-fibroid effect
? protect the immune system
? anti-inflammatory effects
? analgesic effects
? cannabinoids used as anti-itch
? anti-immune suppressive properties
? improve sleep
? improve mood (anti-anxiety)
? improve appetite
? help relieve hardened esophagus
? relieve painful joints

• help with gastrointestinal problems (diarrhea)
• lower blood pressure

Use as adjunct to other prescription drugs.  You may find that you will begin to use less and less of your prescription (NSAIDS and opiates) drugs.  You may be able to cut them out completely.  Medical marijuana will provide relief from many of your symptoms and with little or no side effects.

Best Strains:  Sweet Blu, Dragon, Skywalker x OG Kush,  Headband, Black Domina, Northern Lights, BlackLites, God Bud, Trainwreck, OG Kush.

___________________________________________________________________________________
References:
1. Goldman L, Ausiello D, eds. Cecil Medicine.  23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007.
2. Varga J, Denton CP. Systemic sclerosis and the scleroderma-spectrum disorders.  In: Firestein GS, Budd RC, Harris ED Jr., et al., eds. Kelley's Textbook of Rheumatology.  8th ed. Philadelphia, Pa: Saunders Elsevier; 2008:  chap 77.
3. Clouse RE, Diamant NE. Esophageal motor and sensory function and motor disorders of the esophagus.  In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran's Gastrointestinal and Liver Disease.  8th ed. Philadelphia, Pa: Saunders Elsevier; 2006:  chap 41.

My wheelchair-courtesy The Scooter Store

 

saddle bag

full-weather canopy for PNW weather...  lol

cup holder

close-up  of the "universal cup holder"

Kinda like the connisuer of pot, only in wheelchairs.......

Who is who to judge?

Watch this from my "collection" of videos--][---

She Does NOT show this:

• having to need someone to help you bathe
• what happens when doctors fuck around while your pain becomes entrenched, aka, Independently Mediated Pain!

RSD is never the same-and I hope no one took her advice on "Ice it"

It is you fucking enemy!!!  I had my RSD spread and worsen like wildfire.

What Paula has is a bunch of people paid to say what she wants.

For a little RSD "entertainment"

 had a setback.... 

I am now so bony that we've had to order extra air mattress and...well, I will toss up the photo:

OK, NOW WHAT IS THE BIG DEAL??

BAAAAD DAY!!!!!!!!!!!!!!!!!!!!!!!!

GETTTTING WAAAAAAAAAAAAAAAAY BETTER!!!!!!!!!!!!!!!!!!!!!!!!!!!

 whhhoooaa!


O, speak no more-this needs to be let out and made 100% legal AND covered by the fucking inssssurances.  I dearly hope this experience I am going to video and publish later-start to finish.                                                                                                                  

THE AGONY

What does it mean to have RSD/CRPS?

 Just picture yourself-one day, minding your own business, tending to your yard, chores, household chores, maybe, and you are hanging a photograph, and wham, the hammer connects with your finger instead of your nail in the wall.  Perhaps you yell out and cuss, and maybe are able to consider moving throughout your day, despite the ever increasing crescendo of pain that is building in your thumb, then the next day, it turns into a sharp, burning pain, and you can't handle concentrating on your job even because the wicked burning pain, and now swelling.

Then you notice that the hand you hit with the hammer with is competing with everything you do for your attention, and you feel sick.  Unbeknownst to you, a change has taken hold within your body.  A well-meaning doctor sees the now almost deformed hand, puffed out with swelling and gives you a prescription for 800mg ibuprofen threee times a day, and perhaps about 15 tablets of 5mg oxycodone "take 1-2 every 6-8 hours PRN.  You struggle to stagger the two: but your pain spirals continually out of control, and in 2-3 days, the oxycodone is gone, and you are back at the doctor, but now your hand is two more times the size it was, purple, cold to the doctor's touch, but you feel like it's on fire!!!

Welcome to CRPS/RSD (Complex Regional Pain Syndrome/ formerly known as Reflex Sympathetic Dystrophy).

The only predictibility about it is the unpredictibility.

But in ONE YEAR; this is was RSD did to me: full circle: