Well, I had my "1-month" checkup today following my microdiscectomy operation. The surgeon wants to see me for follow-ups at intervals of 1 month, 3 months, six months and 12 months post-surgery. In addition to checking on me, part of the routine involves filling out forms where I assess my current pain status and describe how the disc problem is affecting my life. I filled out these forms when I first met with the surgeon five months before the operation, then three weeks before, and then on the day of the operation. I guess they keep track of these self-assessments for statistical tracking purposes.
Anyway, I am feeling wonderful! No back pain, no nerve pain down my leg, and I feel like I can do anything! But to be on the safe side I am going to follow all of the restrictions to the letter. Here is a list of things that I still can't do:
- ride the lawnmower (too bumpy)
- use the weed whacker (too heavy/too twisty)
- run (too bumpy)
- swing a baseball bat (too twisty)
- vacuum (too heavy, too twisty)
- carry anything over 15 pounds
On the bright side, here are the things that I can resume doing:
- Total Gym exercises
- floor based core strengthening
and most importantly, now that I can lift more than five pounds, I can play my electric guitars again!
When I talked to the surgeon today, he agreed that my hives were caused by an allergy to chlorhexidine, which was used as the antiseptic wash during my operation. Furthermore, he said that my allergy was a "type 4 reaction", indicating that it was delayed onset (two weeks post-op) and NOT histamine related. Which suddenly explains why I had no relief despite taking two Benadryls every four hours for two weeks (all I got relief from was ice). It turns out that these reactions are related to the T-lymphocytes, and antihistamines are not effective.
I did a little reading on the subject, and found an article that explained this in medical jargon (I've included a quote below). Anyway, after reading about the serious reactions to chlorhexidine (some have died from anaphylactic shock!) I am definitely going to make sure that every doctor and dentist I see in the future knows that I am allergic to this substance.
There are four mechanisms of hypersensitivity, which are classified according to the components of the immune system involved. Type one, hypersensitivity reactions/anaphylactic reactions: This occurs in individuals who have inherited very high levels of a type of antibody called immunoglobulin E (IgE). When exposed to an antigen, these high levels of antibodies activate mast cells and basophils, which release their granular contents. Physiologically the most important substance released is histamine, which constricts smooth muscle within the bronchioles, activates vasodilation and increases vascular permeability (leading to exudation of fluid and proteins into tissues). Examples of type 1 reactions include allergic rhinitis (hay fever), allergic asthma and penicillin-induced anaphylaxis.
Type two, hypersensitivity reactions/cytotoxic hypersensitivity: when an antibody reacts with an antigen on a cell surface, that cell is marked for destruction via a number of mechanisms, for example: phagocytosis, or destruction by lytic enzymes. This is the usual procedure in the elimination of bacteria. If antibodies are directed against self-antigens the result is destruction of the body’s own tissues (autoimmune destruction). Conditions of particular concern within this area are blood transfusion reactions and haemolytic disease of the newborn.
Type three, hypersensitivity reactions/immune complex mediated hypersensitivity: Antibody-antigen complexes are usually cleared efficiently from the blood by phagocytosis. If this process fails; the complexes can be deposited within the body’s tissues, where upon an inflammatory response is initiated. The kidneys are often affected because they receive a large proportion of the cardiac output, and filter the blood. Immune complexes block the glomeruli, impairing renal function (glomerulonephritis). Penicillin sensitivity can also lead to a type three reaction; the body’s antibodies bind to penicillin, which is the offending antigen, the symptoms are the result of deposition of immune complexes in the tissues. Examples include, rashes, joint pains and haematuria. Infectious diseases such as malaria and viral hepatitis can lead to a type three hypersensitivity reaction. This form of hypersensitivity has been implicated in causing systemic lupus erythematosus (SLE) (Taylor and Reide, 1998).
Type four, hypersensitivity reactions/delayed hypersensitivity: unlike the earlier mentioned reactions, type four reactions do not involve antibodies. The reaction is mediated by T-lymphocytes, which overreact to an antigen. When an antigen is detected in the blood it provokes clonal expansion of the T-lymphocyte cells and large numbers of cytotoxic T-lymphocytes are released to terminate the antigen. If the T-lymphocytes are over stimulated and the response becomes inappropriate the aggressive cytotoxic T-lymphocytes will damage normal body cells/tissues. Examples include contact dermatitis, and organ rejection. It is important to note that all of the above hypersensitivity reactions have the potential to induce a state of physiological shock to the individual affected by them.