Hello Wuhdyl,
I?m assuming you are interested in why your son has developed
diabetes-like symptoms, and what is the root of his recurring nausea.
I?d like to address the lab results first. You say the white count
was 7,000, which is normal, but you don?t provide differential
results. When the white count dropped to 2,900, there were atypical
lymphs. Atypical lymphs usually indicate a viral infection, not
bacterial, for which antibiotics will not help. I?d be interested in
the differential results on both sets of hematology (CBC) results.
Scientists are finding evidence that certain viruses can trigger
diabetes. These viruses belong to a group called Enteroviruses, that
attack the intestinal tract. Your son may have been unwittingly
exposed to such a virus, via a bowel nick during the surgery. (More
further down)
You are saying your son has never had elevated blood glucose prior
to this appendectomy? While not definitive for appendectomy, some
patients DO suffer from post operative insulin resistance and surgical
stress. (More further down in the answer. Diabetes can develop, even
with no family history. Is your son overweight? Does he have any other
medical problems?
You don?t say where the Morgagni cyst was located. If it was
abdominal, scar tissue could have developed from surgery.
It does not appear that Augmentin could be at the root of the
persistent nausea or elevated blood glucose. It could be the cause of
a continued fever, if the organism infecting your son is resistant to
Augmentin, a form of penicillin.
Other causes of persistent nausea can be a bowel obstruction, scar
tissue, and surgical site infections, all complications of
laparoscopic surgeries. (More further down)
It *MAY* be that your son is suffering from insulin resistance, due
to infection and stress from the surgery. Or, you son may have been on
the verge of manifesting diabetes and the stress of the surgery
brought it on. I have found no similar cases after an exhaustive
search. Google Answers is unable to diagnose your son?s condition, and
can only provide answers for informational purposes only. I urge you
to have your son evaluated by an endocrinologist who can better seek
the cause for his elevated blood glucose (and ketonuria)
Laparoscopic appendectomies (keyhole type) are not known for causing
elevated blood glucose levels.
Typical post-surgical complications are:
? Bleeding
? Infection
? Removal of a normal appendix
? A leak at the edge of the colon where the appendix was removed
? Injury to adjacent organs such as the small intestine, ureter, or bladder.
? Blood clot to the lungs
Reasons to call the doctor:
? Persistent fever over 101 degrees F (39 C)
? Bleeding
? Increasing abdominal swelling
? Pain that is not relieved by your medications
? Persistent nausea or vomiting
? Chills
? Persistent cough or shortness of breath
? Purulent drainage (pus) from any incision
? Redness surrounding any of your incisions that is worsening or getting bigger
? You are unable to eat or drink liquids
http://www.sages.org/pi_appendectomy.html
http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Appendicectomy?open
Risk Factors
============
Risks of laparoscopic surgery:
What are the Risks of Having Laparoscopic Appendectomy Surgery?
As with any surgery there are risks. The risk of one of these
complications is no greater than if the surgery were done with the
open technique. Complications that can occur are:
? Bleeding
? Infection involving the wound, blood or abdomen
? Injury to surrounding organs such as the bladder, intestines, blood
vessels, or nerves
? Difficulty urinating following surgery may occur and a temporary
catheter may be ordered to drain the bladder
http://www.jmmdhs.com/index.php/laparoscopic_appendix.html
Relative contraindications:
? Complicated appendicitis
? Stump appendicitis
? Poor risk for general anaesthesia
? some cases of previous extensive pelvic surgery
The general anaesthesia and the pneumoperitoneum required as part of
the laparoscopic procedure do increase the risk in certain groups of
patients. Most surgeons would not recommend laparoscopic appendectomy
in those with pre-existing disease conditions. Patients with Cardiac
diseases and COPD should not be considered a good candidate for
laparoscopy. The laparoscopic appendectomy may also be more difficult
in patients who have had previous lower abdominal surgery.?
?There is report also of Mucinous cystadenoma of the cecum missed at
laparoscopic appendectomy. Less than 1% of all patients with suspected
acute appendicitis are found to have an associated malignant process.
During conventional appendectomy through a laparotomy incision, the
caecum and the appendix are easily palpated, and an obvious mass can
be detected and properly managed at the time of appendectomy. The
inability to palpate any mass is an inherent problem of laparoscopic
surgery.
If surgeon is not experienced, the stump of the appendix may be to
long. There is a report of intra-abdominal abscess formation due to
retained faecolith after laparoscopic appendectomy. It is strongly
advised that the surgeons performing laparoscopic appendectomy should
remove faecolith if found, and the stump of appendix should not big
enough to contain any thing. Incomplete appendectomy is a result of
ligation of the appendix too far from the base. It may lead to
recurrent appendicitis, which presents with symptoms and signs of
appendicitis even after laparoscopic appendectomy. Leakage of purulent
exudates from appendix at the time of operation.?
http://www.laparoscopyhospital.com/lap%20app.htm
?Studies examining risk factors for postoperative infections (eg,
wound infection and pneumonia) found obesity, among others, as an
independent risk factor [16,32-34]. Individuals who are morbidly obese
have multiple comorbidities, including insulin resistance and
pulmonary dysfunction, which indirectly increases their risk for
infectious complications. Chronic hyperglycemia in patients with
diabetes has been shown to increase multiple postoperative
complications, including infection [35-39,40?]. It is likely that
there is an increased risk for infection in patients who are not
diabetic who experience profound hyperglycemia postoperatively.
A prospective, randomized, controlled study of critically ill
patients in a surgical intensive care unit demonstrated a 46%
reduction in bloodstream infections through intensive glucose control
with exogenous insulin administration [35]. Oxygen tension in tissue
strongly influences the incidence of surgical wound infections
[41,42]. Bactericidal activity of neutrophils, a critical defense
against microbial pathogens, is dependent on the production of
superoxide radicals, a process limited by partial pressure of oxygen
in tissue [43,44]. The surgical disruption of arterial supply of a
poorly vascularized, thick layer of adipose tissue, combined with
hypoxemia from sleep apnea, obesity-induced hypoventilation, and
pulmonary dysfunction, increase the morbidly obese patient's risk for
wound infections. Therefore, patients who are morbidly obese have
direct and indirect risk factors for postoperative infections.?
http://www.biomedcentral.com/1523-3820/5/387
Small Bowel Obstruction
========================
?According to Zbar et al, the most common operative procedure
associated with a subsequent small bowel obstruction is appendectomy
with an incidence of 10.7% during a follow-up period of 5.3 years. In
the study, small bowel obstruction occurred more frequently in the
first 40 months after appendectomy and in those individuals who
underwent appendectomy for ruptured appen-dicitis.2 Since small bowel
obstructions occur more frequently in the earlier years after
appendectomy, patients who present with non-specific initial symptoms
(fever, nausea, vomiting, abdominal pain) years after appendectomy may
be misdiagnosed in the early stage of the condition?
http://www.med.ucla.edu/modules/wfsection/article.php?articleid=107
?A small-bowel obstruction (SBO) is caused by a variety of pathologic
processes. The leading cause of SBO in developed countries is
postoperative adhesions (60%) followed by malignancy, Crohn disease,
and hernias, although some studies have reported Crohn disease as a
greater etiologic factor than neoplasia. Surgeries most closely
associated with SBO are appendectomy, colorectal surgery, and
gynecologic and upper gastrointestinal (GI) procedures. One study from
Canada reports a higher frequency of SBO after colorectal surgery,
followed by gynecologic surgery, hernia repair, and appendectomy.
Lower abdominal and pelvic surgeries lead to obstruction more often
than upper GI surgeries.
SBOs can be partial or complete, simple (ie, nonstrangulated) or
strangulated. Strangulated obstructions are surgical emergencies. If
not diagnosed and properly treated, vascular compromise leads to bowel
ischemia and further morbidity and mortality. Because as many as 40%
of patients have strangulated obstructions, differentiating the
characteristics and etiologies of obstruction is critical to proper
patient treatment.
Pathophysiology: Obstruction of the small bowel leads to proximal
dilatation of the intestine due to accumulation of GI secretions and
swallowed air. This bowel dilatation stimulates cell secretory
activity resulting in more fluid accumulation. This leads to increased
peristalsis both above and below the obstruction with frequent loose
stools and flatus early in its course.
Vomiting occurs if the level of obstruction is proximal. Increasing
small-bowel distention leads to increased intraluminal pressures. This
can cause compression of mucosal lymphatics leading to bowel wall
lymphedema. With even higher intraluminal hydrostatic pressures,
increased hydrostatic pressure in the capillary beds results in
massive third spacing of fluid, electrolytes, and proteins into the
intestinal lumen. The fluid loss and dehydration that ensue may be
severe and contribute to increased morbidity and mortality.
Strangulated SBOs are most commonly associated with adhesions and
occur when a loop of distended bowel twists on its mesenteric pedicle.
The arterial occlusion leads to bowel ischemia and necrosis. If left
untreated, this progresses to perforation, peritonitis, and death.
Bacteria in the gut proliferate proximal to the obstruction.
Microvascular changes in the bowel wall allow translocation to the
mesenteric lymph nodes. This is associated with an increase in
incidence of bacteremia due to Escherichia coli, but the clinical
significance is unclear.?
http://www.emedicine.com/EMERG/topic66.htm
Insulin Resistance
===================
?In surgical patients insulin resistance has been characterized in
some detail, and has been shown to have many similarities with
metabolic changes seen in patients with type 2 diabetes. This finding
may be important since insulin resistance has been shown to be one
independent factor that influences length of stay. When patients about
to undergo elective surgery have been treated with glucose
intravenously or a carbohydrate-rich drink instead of overnight
fasting, insulin resistance was reduced by about half.
A small meta-analysis showed that when post-operative insulin
resistance was reduced by pre-operative carbohydrates, length of
hospital stay was shortened. Overnight intravenous glucose at high
doses improved post-operative N economy. This type of treatment has
also been shown repeatedly to reduce cardiac complications after
open-heart surgery. Furthermore, if the carbohydrates are given as a
drink pre-operatively, pre-operative thirst, hunger and anxiety are
markedly reduced. In summary, preventing or treating insulin
resistance in surgical stress influences outcome. Fasting overnight is
not an optimal way to prepare patients for elective surgery. Instead,
pre-operative carbohydrates have clinical benefits.?
http://www.ingentaconnect.com/content/cabi/pns/2002/00000061/00000003/art00002
?Furthermore, gastrointestinal instability provoked by anesthesia,
medications, and stress-related vagal overlay can lead to nausea,
vomiting, and dehydration. This compounds the volume contraction that
may already be present from the osmotic diuresis induced by
hyperglycemia, thereby increasing the risk for ischemic events and
acute renal failure. Subtle to gross deficits in key electrolytes
(principally potassium, but also magnesium) may pose an arrhythmogenic
risk, which often is superimposed on a milieu of endemic coronary
artery disease in middle-aged or older people with diabetes.?
?In addition to insulin resistance induced by circulating stress
hormones, surgical stress has a deleterious effect on pancreatic
ß-cell function. Plasma insulin levels fall, and insulin secretory
responses to glucose become impaired during surgery.17?19 The
mechanism of the impaired ß-cell responsiveness during surgery is
unclear, and the defect is poorly correlated with ambient
intraoperative catecholamine levels. Postoperatively, however, there
is a close inverse correlation between plasma epinephrine and insulin
secretion.1?
?These anti-insulin effects of the metabolic stress response
essentially reverse the physiological anabolic and anti-catabolic
actions of insulin. The important anabolic actions of insulin that may
be reversed or attenuated during the stress of surgery include: 1)
stimulation of glucose uptake and glycogen storage, 2) stimulation of
amino acid uptake and protein synthesis by skeletal muscle, 3)
stimulation of fatty acid synthesis in the liver and storage in
adipocytes, and 4) renal sodium reabsorption and intravascular volume
preservation.
The anti-catabolic effects of insulin include: 1) inhibition of
hepatic glycogen breakdown, 2) inhibition of gluconeogenesis, 3)
inhibition of lipolysis, 4) inhibition of fatty acid oxidation and
ketone body formation, and 5) inhibition of proteolysis and amino acid
oxidation. Thus, inhibition of insulin secretion and action shifts the
perioperative milieu toward hypercatabolism through a variety of
mechanisms.?
?These effects predispose to severe hyperglycemia, which is further
exacerbated by the stimulatory effect of epinephrine and
norepinephrine on glucagon secretion. Other catabolic effects of
catecholamines include stimulation of lipolysis and ketogenesis.
Epinephrine increases adipocyte cAMP levels, leading to
phosphorylation and activation of hormone-sensitive lipase. The
activated hormone-sensitive lipase promotes lipolysis and release of
free fatty acids into the circulation.?
http://spectrum.diabetesjournals.org/cgi/content/full/15/1/44
?Critical illness is associated with a marked increase in metabolic
rate and progressive wasting, despite aggressive nutritional support.
The metabolic events which are responsible for these phenomena are
unclear, but are characterised by marked impairment of the anabolic
effects of insulin on glucose metabolism and excessive activation of
the sympathetic nervous system. It has been suggested that critical
illness may be associated with impaired carbohydrate oxidation and a
marked increase in the loss of heat energy associated with glucose
administration (glucoseinduced thermogenesis).
This situation may result in impaired efficiency of nutrient
assimilation. Studies employing combinations of nutrient infusions
both at clinically-relevant rates and in association with euglycaemic
hyperinsulinaemia have, however, demonstrated that nutrientinduced
thermogenesis is unaffected in critical illness in human subjects, and
that defective glucose utilization occurs as a consequence of impaired
insulin-mediated glucose storage rather than oxidation.?
http://www.cabi-publishing.org/Pdf/SampleJournals/pns60381.pdf
?The syndromes of insulin resistance actually comprise a broad
clinical spectrum. These include patients with obesity, glucose
intolerance, diabetes, syndrome X, and also patients with an extreme
insulin-resistant state. Many of these disorders are associated with
various endocrine, metabolic, and genetic conditions. The syndromes
also may be associated with immunological diseases and may exhibit
distinct phenotypic characteristics.?
?The mechanisms that are responsible for the insulin resistance
syndromes (IRS) include genetic or primary target cell defects,
autoantibodies to insulin, and accelerated insulin degradation.
Obesity, the most common cause of insulin resistance, is associated
with a decreased number of receptors and postreceptor failure to
activate the tyrosine kinase.
Insulin resistance plays a major pathogenic role in the development
of the metabolic syndrome that may include any or all of the
following: hyperinsulinemia; type 2 diabetes or glucose intolerance;
central obesity; hypertension; dyslipidemia that includes high
triglycerides (TG); low high-density lipoprotein cholesterol (HDL-C)
and small, dense low-density lipoprotein (LDL) particles; and
hypercoagulability characterized by an increased plasminogen activator
inhibitor-1 (PAI-1) level.
Insulin resistance, the compensatory hyperinsulinemia, and other
components are associated with increased risk of cardiovascular
disease; endothelial dysfunction is a prominent feature of the IRS.
Type 2 diabetes is characterized by increased hepatic glucose output,
increased peripheral resistance to action of insulin caused by
receptor and postreceptor defects, and impaired insulin secretion. In
skeletal muscle, insulin resistance may be caused by various
abnormalities, including defective glucose transport. Glucose
transporter (GLUT)-4 is the main insulin-responsive transporter.
Insulin and IGFs are important regulators of ovarian function.
Insulin resistance and hyperinsulinemia are thought to be responsible
for the hyperandrogenism that is characteristic of polycystic ovary
disease (PCOD). Other distinct manifestations of the IRS or related
conditions involve various organs, as well as the skin.
Two major variants of insulin receptor abnormalities that are
associated with acanthosis nigricans have been described?the classic
type A insulin resistance syndrome due to absent or dysfunctional
receptor and type B resulting from autoantibodies to insulin receptor.
Both are associated with hyperinsulinemia. Hypoglycemia may still
occur in some individuals with IRS because of an agonist effect of
autoantibodies on the insulin receptor. In some other patients with
insulin-binding antibodies, when insulin dissociates from the
antibodies several hours after a meal, hypoglycemia may occur.?
?Insulin resistance results from inherited and acquired influences.
Hereditary causes include mutations of insulin receptor, glucose
transporter, and signaling proteins, although the common forms largely
are unidentified. Acquired causes include physical inactivity, diet,
medications, hyperglycemia (glucose toxicity), increased free fatty
acids, and the aging process.
The underlying causes of insulin-resistant states can be categorized as follows:
? Prereceptor
o Abnormal insulin (mutations)
o Anti-insulin antibodies
? Receptor
o Decreased number of receptors, mainly failure to activate tyrosine kinase
o Reduced binding of insulin
o Insulin receptor mutations
o Insulin receptor?blocking antibodies
? Postreceptor
o Defective signal transduction
o In theory, mutations of glucose transporter (GLUT)-4 could cause
insulin resistance, but polymorphisms in the GLUT-4 gene are very rare
in patients.
http://www.emedicine.com/med/topic1173.htm
?Significant differences were revealed in the mechanism of
hyperglycemia in extensive wounds and generalized surgical infection.
Hyperglycemia in extensive burn injuries is caused by the inhibition
of insulin formation, decreased insulin binding to cellular receptors,
which leads to decreased sensitivity of tissues to insulin.
Hyperglycemia developing in generalized infection is a result of
insufficient blood insulin levels consequent to inhibition of its
secretion (while insulin biosynthesis is elevated) under the effects
of hyperproduction of prostaglandins, and is also mediated by defects
in insulin-receptor interaction. Correction of carbohydrate metabolism
disorders in these surgical pathologies in spite of the different
pathogenetic mechanisms might be achieved by exogenous insulin
administration, and also by insulin administration together with
indomethacin, a nonsteroid anti-inflammatory agent, inhibiting
prostaglandin production.?
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3307258&dopt=Abstract
?What role does genetics have in the development of type 2 diabetes?
There is no doubt that genes play a role in determining risk for
diabetes. The lifetime risk for developing diabetes is about 40
percent if you have a first-degree relative with type 2 diabetes and
goes up to over 80 percent if you have an identical twin with
diabetes. We also think the higher rates of diabetes in certain ethnic
groups, such as African Americans, Hispanic Americans and Native
Americans, is explained by differences in genes in these groups?
?Insulin resistance is a condition that develops when people become
obese. It is characterized by a less than normal response to insulin,
the hormone produced by the body to help it use sugar. Most people
with insulin resistance do not develop diabetes, but it can have other
harmful effects, such as increasing risk for heart attacks. Lifestyle
changes such as increasing physical activity and losing weight can
improve insulin resistance.?
http://www.burlingtonfreepress.com/health/news_trends2.htm
Adhesions, scar tissue, SSI (Surgical Site Infections)and Viruses:
==================================================================
?SSIs can be classified as incisional and organ/space manipulated
during an operation. Incisional infections are further divided in
superficial (skin and subcutaneous tissue) and deep (deep soft tissue
muscle and fascia). Deep incisional and organ/space are the types of
SSIs that cause the most morbidity. Definitions of SSIs can be found
in the Centers for Disease Control and Prevention (CDC)'s Guideline
for Prevention of Surgical Site Infection, 1999.?
?There is evidence to show a relationship between hyperglycemia
(glucose greater than 200) during the first 48 hours following surgery
and an increased risk of SSI.7 In addition, in a prospective,
sequential study of 2,467 diabetic patients undergoing cardiac surgery
from 1987 to 1997, those who received intermittent subcutaneous
insulin had a higher rate of deep sternal SSI than those who received
continuous intravenous insulin during the procedure (2.0 percent vs.
0.8 percent p=.01)8
These two studies show that tight control of blood glucose levels in
the perioperative period may lead to better SSI outcomes in diabetic
and non-diabetic patients.?
http://www.infectioncontroltoday.com/articles/241feat1.html
?Abdominal adhesions are bands of fibrous scar tissue that form on
abdominal organs, causing the organs to stick to one another or to the
wall of the abdomen. In people living in developed countries,
adhesions most commonly develop after abdominal surgery, in which
organs are handled by the surgical team and are shifted temporarily
from their normal positions. Similar scarring can occur in people who
develop peritonitis, the spread of an abdominal infection to the
membrane that covers the abdominal organs. Peritonitis can occur after
appendicitis or another abdominal infection. Other causes of adhesions
include endometriosis, an inflammatory condition that affects some
women and may involve the abdomen and serious abdominal trauma.?
?When more significant intestinal obstruction develops, the following
symptoms can occur:
? Severe, crampy abdominal pain
? Nausea and vomiting
? Swelling of the abdomen (abdominal distension)
? Inability to pass gas and absent or infrequent bowel movements
? Signs of dehydration, including dry skin, dry mouth and tongue,
severe thirst, infrequent urination, fast heart rate and low blood
pressure
http://www.intelihealth.com/IH/ihtIH/WSIHW000/9339/9414.html
?Type 1 Diabetes usually develops due to an autoimmune disorder. This
is when the body's immune system behaves inappropriately and starts
seeing one of it's own tissues as foreign. In the case of Type 1
Diabetes, the islet cells of the pancreas that produce insulin are
seen as the "enemy" by mistake. The body then creates antibodies to
fight the "foreign" tissue and destroys the islet cells ability to
produce insulin.
The lack of sufficient insulin thereby results in diabetes. It is
unknown why this autoimmune diabetes develops. Most often it is a
genetic tendency. Sometimes it follows a viral infection such as
mumps, rubella, cytomegalovirus, measles, influenza, encephalitis,
polio or Epstein-Barr virus. Certain people are more genetically prone
to this happening although why this occurs is not know. Thus, two
people may be infected with the same virus and only one of them who is
genetically prone will go on to develop diabetes. Other less common (
very rare) causes of Type 1 Diabetes include injury to the pancreas
from toxins, trauma, or after the surgical removal of the majority (or
all) of the pancreas.?
http://www.endocrineweb.com/diabetes/1diabetes.html
?Researchers in California and Florida have strong new evidence
implicating a common class of viruses in causing Type 1 or
insulin-dependent diabetes, a discovery that eventually could lead to
ways of preventing the disease that affects as many as 1 million
Americans.
Type 1 diabetes occurs when the body's immune system attacks and
destroys insulin-producing cells in the pancreas. Researchers know
that only people with a specific genetic profile are susceptible to
this autoimmune attack, but there has been debate about the identity
of the agent that triggers the immune reaction.
Now, two studies in this month's issues of the Journal of Experimental
Medicine and the Journal of Clinical Investigation strongly implicate
coxsackie viruses, polio-related viruses that cause upper respiratory
infections.
One report shows that coxsackie viruses trigger diabetes in
genetically susceptible mice but not in those that have a different
genetic profile. The second demonstrates that the autoimmune reaction
is triggered by a similarity between a coxsackie virus protein and a
protein in the pancreas.?
http://www.childrenwithdiabetes.com/d_0n_120.htm
?Certain factors are thought to be important in this process:
? White blood cells called T lymphocytes produce immune factors called
cytokines that attack and gradually destroy the beta cells of the
pancreas. Important cytokines are interleukin-1beta, tumor necrosis
factor-alpha, and interferon-gamma.
? Specific proteins are also critical in the process. They include
glutamic acid decarboxylase (GAD), insulin, and islet cell antigens.
These proteins serve as autoantigens. That is, they trigger the
self-attack of the autoantibodies on the body's own beta cells.
Progression from the first stage, known as insulitis, to full-blown
diabetes can take seven years or longer. Unfortunately, by the time a
person is aware that something is wrong and goes to the doctor with
symptoms of type 1 diabetes, about 80% to 90% of the beta cells have
been destroyed.
It should be noted that more than half of those with insulitis does
not develop diabetes. Researchers are greatly interested in
discovering any factors that prevent the disease.?
?Some researchers believe one or more viral infections may trigger the
disease in genetically susceptible individuals. Researchers suggest
the following scenario:
? An infection introduces a viral protein that resembles a beta-cell protein.
? T cells and antibodies are tricked by this resemblance into
attacking the beta protein as well as the virus.
Among the viruses under scrutiny are enteric viruses, which attack the
intestinal tract. Coxsackieviruses are an enteric virus of particular
interest. (One study has suggested that respiratory infection in a
child's first year, and not later, may be protective against diabetes,
perhaps by priming the immune response so that it is better able to
respond later on to other organisms.)?
http://www.umm.edu/patiented/articles/what_causes_type_1_diabetes_000009_2.htm
Lost staples (?????)
?Laparoscopic linear cutting staplers are commonplace in advanced
laparoscopic techniques. Most of the loose staples are probably inert,
but we present a case of a mechanical small bowel obstruction after a
laparoscopic appendectomy. The etiology of the bowel obstruction was a
loose linear cutter staple from the load that fired across the
appendiceal stump. We recommend retrieving as many loose staples as
possible with the laparoscopic grasper or suction at the termination
of the laparoscopy.?
http://www.surgical-laparoscopy.com/pt/re/slept/abstract.00129689-200208000-00019.htm;jsessionid=DE00v2y2XA11UsfxKfFdfT24EjTu2weDEjs898sUoBLqj4jNoBK6!784801133!-949856144!9001!-1
Augmentin
==========
? Other, less serious side effects may be more likely to occur.
Continue to take Augmentin and talk to your doctor if you experience
? mild diarrhea;
? nausea or vomiting;
? rash;
? white patches in the mouth (thrush/yeast infection); or
? vaginal yeast infection or diaper rash.
? Side effects other than those listed here may also occur. Talk to
your doctor about any side effect that seems unusual or that is
especially bothersome.
http://www.drugs.com/augmentin.html
Management
==========
Your son should be evaluated by a competent endocrinologist, who
can determine the cause and management of your son?s medical
condition. The endocrinologist will be familiar with your son?s entire
medical history, and can order a HbgA1c test and insulin
auto-antibodies to get a better picture of what is causing his
hyperglycemia. Possibly testing for Crohn?s disease may be warranted.
Hopefully the hyperglyemia will be transient. Perhaps a regimen of a
different course of antibiotics, a broad spectrum antibiotic will help
if bacterial infection is still present.
http://www.diabetesforum.net/eng_treat_insulin_antibodies.htm
What is a HgbA1c test?
----------------------
?This is a test that is done in a lab to determine your overall blood
glucose level control. Hemoglobin is found inside red blood cells. Its
job is to carry oxygen from the lungs to all the cells in the body.
When you have uncontrolled diabetes the extra glucose in your
bloodstream enters the red blood cells and links up (or glycates) with
molecules of hemoglobin.
Each molecule stays glycated until that red blood cell dies and is
replaced with a new red blood cell. The amount of glycated hemoglobin
in your blood shows the average blood glucose control for the past
three to four months, which is the lifespan of a red blood cell.
In a person who does not have diabetes, about 5% of all hemoglobin is
glycated. For someone with diabetes the levels can range from 5% to as
high as 25% if their diabetes is badly out of control for a long time.
If you use insulin you should have this test done four times a year.?
http://www.healthtouch.com/diabetesplace/ask-testing.asp?cid=HTFEAT&cname=Healthtouch
An Aside:
?For 33 years after his 1923 appendectomy, Eisenhower had episodic
lower abdominal pain. The diagnosis of partial small bowel obstruction
was entertained in a November 1947 episode, which ultimately resolved
spontaneously. In May 1956 a small bowel series led to the diagnosis
of regional enteritis (Crohn disease) affecting the terminal ileum.
http://www.doctorzebra.com/prez/t34.htm
I hope this helps you and your son. If any part of this answer is
unclear, please request an Answer Clarification, before you rate. This
will enable me to assist you further, if possible.?
I wish your son and you the best.
Sincerely, Crabcakes
Search Terms
============
hyperglycemia + appendectomy
SSI + appendectomy
surgical site infection + insulin resistance
surgery induced + hyperglycemia
surgery induced + diabetes
insulin autoantibodies
laparoscopic appendectomy risks
laparoscopic appendectomy complications + diabetes
jejunoduodenal junction + hyperglycemia
bowel obstruction after appendectomy
bowel piercing + infection appendectomy |
