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Claims  |
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What is claimed and desired to be secured by United States Letters Patent
is:
1. A subcutaneous conduit for injecting a drug into a peritoneal cavity,
comprising:
an injection receiver having a diametrally enlarged, convergent receiving
surface and an opening in the receiving surface;
a diametrally enlarged, penetrable cover across the receiving surface in
spaced relationship therewith, the cover forming a receiving reservoir in
combination with the receiving surface;
a hollow stem having a proximal end and a distal end, the proximal end of
the stem being attached to the injection receiver such that the stem forms
a passageway extending from the opening in the receiving surface, the stem
having a length sufficient that the stem penetrates the parietal
peritoneal membrane and extends into the peritoneal cavity; and
a diametrally enlarged flange attached to the stem such that, when the
conduit is implanted under a layer of skin adjacent the peritoneal cavity
and the flange is secured adjacent the parietal peritoneal membrane, the
distal end of the hollow stem is directed toward the mesenteric peritoneal
membrane.
2. A subcutaneous conduit as defined in claim 1 wherein the injection
receiver comprises a penetration-resistant material.
3. A subcutaneous conduit as defined in claim 1 wherein the injection
receiver comprises a generally circular periphery around the convergent
receiving surface and a raised rim circumscribing the periphery, the rim
assisting the cover in defining the receiving reservoir.
4. A subcutaneous conduit as defined in claim 3 wherein the injection
receiver further comprises an annular shelf below the rim and the cover
comprises an annular lip that is engagedly received by the shelf.
5. A subcutaneous conduit as defined in claim 1 wherein the diametrally
enlarged flange is attached adjacent the distal end of the hollow stem,
the flange thereby inhibiting the stem from retracting into tissue into
which the conduit is implanted.
6. A subcutaneous conduit as defined in claim 1 wherein the injection
receiver includes a bore which is countersunk into the receiver from the
side opposite the convergent surface, the countersunk bore receiving the
hollow stem with the passageway in alignment with the opening.
7. A subcutaneous conduit as defined in claim 1 wherein the penetrable
cover is fabricated from a resilient material and with a dome-like
configuration, the dome extending away from the receiving surface.
8. A subcutaneous conduit as defined in claim 1 wherein the cover comprises
a circumferential groove, the groove serving a a channel for receiving a
suture means, the suture means securing the cover to the injection
receiver.
9. A subcutaneous conduit as defined in claim 1 wherein the conduit
comprises a velour covering over at least a portion of the external
surface of the conduit, the velour covering comprising a biocompatible
material and providing for tissue ingrowth into the velour material.
10. A subcutaneously implantable injection conduit for injecting a drug
into a peritoneal cavity, comprising:
a hollow receptacle for receiving the drug, the hollow receptacle being
formed as an open-top chamber;
a penetrable membrane over the open top of the chamber;
a hollow stem having a proximal end and a distal end, the proximal end of
the stem being attached to the receptacle such that the stem forms a
passageway extending from the chamber, the stem having a length sufficient
that the stem penetrates the parietal peritoneal membrane and extends into
the peritoneal cavity;
a diametrally enlarged flange attached to the stem such that, when the
conduit is implanted under a layer of skin adjacent the peritoneal cavity
and the flange is secured adjacent the parietal peritoneal membrane, the
distal end of the hollow stem is directed toward the mesenteric peritoneal
membrane; and
mounting means for mounting the receptacle under a layer of skin adjacent
the peritoneal cavity.
11. A subcutaneously implantable injection conduit as defined in claim 10
wherein the receptacle comprises a cavity formed as an inverted, right
frustoconical vessel having a diameter greater than depth with a circular
base forming the open top of the chamber and connected at the apex of the
frustoconical vessel to the hollow stem.
12. A subcutaneously implantable injection conduit as defined in claim 10
wherein the receptacle comprises a funnel-shaped receiver and the hollow
stem is mounted to the apex of the funnel-shaped receiver.
13. A subcutaneously implantable injection conduit as defined in claim 12
wherein the apex of the funnel-shaped receiver includes a countersunk bore
and the hollow stem is telescopically mounted in the bore.
14. A subcutaneously implantable injection conduit as defined in claim 13
wherein the hollow stem is fabricated from a suitable material to
accommodate the hollow stem being adjustable in length.
15. A subcutaneously implantable injection conduit as defined in claim 10
wherein the diametrally enlarged flange is attached adjacent the distal
end of the hollow stem, the flange thereby inhibiting the stem from
retracting into tissue into which the conduit is implanted.
16. A subcutaneously implantable injection conduit as defined in claim 10
wherein the mounting means comprises a velour covering over the injection
conduit, the velour accommodating tissue ingrowth.
17. A subcutaneously implantable injection conduit as defined in claim 10
wherein the penetrable membrane is fabricated with a dome configuration
from a resilient material, the dome allowing the penetrable membrane to be
depressed to expel the drug from the receptacle.
18. A method for injecting a drug into a peritoneal cavity in a direction
toward the mesenteric peritoneal membrane, the method comprising the steps
of:
obtaining an injection conduit, comprising:
a shallow vessel with an open top; a penetrable membrane covering the open
top of the vessel;
a hollow stem having a proximal end and a distal end, the proximal end of
the stem being attached to the vessel such that the stem forms a
passageway extending from the vessel; and
a diametrally enlarged flange attached to the stem such that, when the
conduit is implanted underneath a layer of skin adjacent the peritoneal
cavity and the flange is secured adjacent the parietal peritoneal
membrane, the distal end of the hollow stem is directed toward the
mesenteric peritoneal membrane;
implanting the injection conduit underneath a layer of skin adjacent the
peritoneal cavity with the membrane being generally parallel to the skin,
the hollow stem penetrating the parietal peritoneal membrane and extending
into the peritoneal cavity, the diametrally enlarged flange being secured
adjacent the parietal peritoneal membrane, the distal end of the hollow
stem being directed toward the mesenteric peritoneal membrane, and the
passageway communicating between the vessel and the peritoneal cavity; and
injecting a drug into the peritoneal cavity by penetrating the layer of
skin and the penetrable membrane with a hollow needle and forcing the drug
through the hollow needle into the vessel with the hollow stem carrying
the drug into the peritoneal cavity in a direction toward the mesenteric
peritoneal membrane.
19. A method as defined in claim 18 wherein the implanting step further
comprises securing the hollow stem in the peritoneal cavity thereby
preventing dislodgement of the hollow stem.
20. A method as defined in claim 18 wherein the injection circuit further
comprises a biocompatible velour material covering at least a portion of
the injection conduit, the biocompatible velour material providing for
tissue ingrowth into the velour material after implanting the injection
conduit.
21. A method as defined in claim 18 wherein the vessel is fabricated from a
puncture-resistant material.
22. A method as defined in claim 18 wherein the diametrally enlarged flange
is attached adjacent the distal end of the stem, the flange thereby
inhibiting the stem from retracting into tissue into which the injection
conduit is implanted.
23. A method as defined in claim 18 wherein the penetrable membrane is
fabricated from a resilient material and with a dome-like configuration,
the dome extending away from the vessel.
24. A method as defined in claim 23 wherein the injecting step further
comprises selectively, manually depressing the dome thereby expelling the
drug from the vessel into the peritoneal cavity in a direction toward the
mesenteric peritoneal membrane.
25. A method as defined in claim 24 wherein the depressing step comprises
manually releasing the dome, the resilient material returning the dome to
its dome-like configuration and repeating the depressing step thereby
flushing the vessel.
26. A method as defined in claim 18 wherein the vessel comprises a
diametrally enlarged convergent receiving surface.
27. A method as defined in claim 18 wherein the drug is insulin and wherein
the insulin, upon entering the peritoneal cavity through the hollow stem
so as to contact the mesenteric peritoneal membrane, is absorbed into the
blood circulation of the portal venous system via said mesenteric
peritoneal membrane, whereby the insulin is transported directly to the
liver.
28. A peritoneal catheter comprising:
a body having a diametrally enlarged, convergent receiving surface and
having an opening in the receiving surface, a periphery around the
receiving surface, a raised rim circumscribing the periphery, and a shelf
below the rim;
a hollow stem attached to the body, the stem forming a passageway extending
from the opening; and
a diametrally enlarged, penetrable cover across the receiving surface in
spaced relationship therewith, the cover being assisted by the rim in
forming a receiving reservoir in combination with the receiving surface,
and the cover having a lip that is engagedly received by the shelf.
29. An implantable peritoneal injection catheter, comprising:
a body having a penetration-resistant, diametrally enlarged, convergent
receiving surface and an opening at the center of the receiving surface,
said body comprising a circular periphery around the convergent receiving
surface, a raised rim circumscribing the periphery, an annular shelf below
the rim, and a bore which is countersunk into the body from the side
opposite the convergent surface such that the countersunk bore is in
alignment with the opening;
a diametrally enlarged, penetrable cover across the receiving surface in
spaced relationship therewith, the cover being assisted by the raised rim
in forming a receiving reservoir in combination with the receiving
surface, the cover comprising an annular lip that is engagedly received by
the shelf, and the cover being fabricated from a resilient material and
having a dome-like configuration, the dome extending away from the
receiving surface; and
a hollow stem having a proximal end and a distal end, the proximal end of
the stem being telescopically received into the countersunk bore such that
the stem forms a passageway extending from the opening, the distal end of
the stem being formed as a diametrally enlarged flange, and the stem
having a predetermined length such that, when the catheter is implanted
under a layer of skin adjacent to a peritoneal cavity, the stem extends
from the body into the peritoneal cavity with the distal end of the stem
being inside the peritoneal cavity and the enlarged flange residing
against a wall of the peritoneal cavity so as to surround a point on the
wall of the peritoneal cavity through which the stem enters the peritoneal
cavity, the stem thereby accommodating fluid communication into the
peritoneal cavity, and the flange inhibiting the stem from retracting into
tissue into which the catheter is implanted.
30. The implantable peritoneal injection catheter defined in claim 29
wherein the cover further comprises a circumferential groove, the groove
serving as a channel for receiving a suture means, the suture means
securing the cover to the body.
31. The implantable peritoneal injection catheter defined in claim 29
further comprising means for mounting the catheter under a layer of skin
adjacent to the peritoneal cavity, said mounting means comprising a
biocompatible velour covering over at least a portion of the external
surface of the peritoneal catheter, the velour covering providing for
tissue ingrowth into the velour material.
32. A subcutaneously implantable injection conduit for injecting insulin
into a peritoneal cavity in a direction toward the mesenteric peritoneal
membrane, comprising:
an injection receiver having a penetration-resistant, diametrally enlarged,
convergent receiving surface and an opening at the center of the receiving
surface, said injection receiver comprising a circular periphery around
the convergent receiving surface, a raised rim circumscribing the
periphery, an annular shelf below the rim, and a bore which is countersunk
into the injection receiver from the side opposite the convergent surface
such that the countersunk bore is in alignment with the opening;
a diametrally enlarged, penetrable cover across the receiving surface in
spaced relationship therewith, the cover being assisted by the raised rim
in forming a receiving reservoir in combination with the receiving
surface, the cover comprising an annular lip that is engagedly received by
the annular shelf, and the cover being fabricated from a resilient
material and having a dome-like configuration, the dome extending away
from the receiving surface;
a hollow stem having a proximal end and a distal end, the proximal end of
the stem being telescopically received into the countersunk bore in the
injection receiver such that the stem forms a passageway extending from
the opening in the receiving surface, and the stem having a length
sufficient that, when the injection conduit is implanted in tissue
adjacent the peritoneal cavity, the stem penetrates the parietal
peritoneal membrane and extends from the injection receiver into the
peritoneal cavity; and
a diametrally enlarged flange attached adjacent the distal end of the
hollow stem such that the flange inhibits the stem from retracting into
tissue into which the conduit is implanted, and such that, when the flange
is secured adjacent the parietal peritoneal membrane, the distal end of
the stem is directed toward the mesenteric peritoneal membrane, whereby
the insulin, upon entering the peritoneal cavity through the hollow stem,
contacts the mesenteric peritoneal membrane and is absorbed into the blood
circulation of the portal venous system via said mesenteric peritoneal
membrane, whereby the insulin is transported directly to the liver.
33. A subcutaneously implantable injection conduit as defined in claim 32
further comprising means for mounting the conduit in tissue adjacent the
peritoneal cavity, said mounting means comprising a biocompatible velour
covering over at least a portion of the external surface of the conduit,
the velour covering providing for tissue ingrowth into the velour
material. |
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Claims |
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Description |
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BACKGROUND
1. Field of the Invention
This invention relates to injection catheters and, more particularly, to a
novel subcutaneous peritoneal injection catheter apparatus and method for
providing injection access to the peritoneal cavity.
2. The Prior Art
Glucose is a major fuel for the body with the brain being the notable
consumer. Insulin is required by many, but not all, tissues for the uptake
and/or utilization of glucose.
The liver and pancreas are the pivotal organs in glucose control with
insulin serving as a vital regulatory hormone. For example, in response to
rising levels of glucose, the pancreatic beta cells secrete insulin which
travels from the pancreas to the portal vein and then to the liver where
the liver extracts approximately 50 percent of the insulin. The remaining
50% of the insulin then travels throughout the rest of the body to
specific receptors in other tissues. In response to insulin, the liver
commences storage of glucose in the form of glycogen (a starch). In the
fasting state, the liver releases a steady output of this stored glucose
thereby supplying many body tissues with their requisite amounts of
glucose.
Conversely glucose utilization by other tissues is insignificantly affected
by normal pancreatic insulin secretion. It has been stated that the
greater response of the liver as compared to peripheral tissues (fat and
muscle) to small changes in insulin levels need not reflect an inherently
greater sensitivity on the part of the liver cell (hepatocyte), rather, it
may be a consequence of high ambient levels of endogenous (self-produced)
insulin in portal as compared to peripheral blood. In summary, therefore,
the major effect of insulin in a normal human is to lower the blood
glucose levels by decreasing the rate of glucose output by the liver.
Diabetics suffer from relative or absolute deficiency in insulin secretion
(resulting in high blood sugar levels) and tissue cells which are
"starving" for glucose yet are unable to "feed" (absorb glucose) in the
absence of insulin. Historically, the treatment has been to provide
insulin by injections into the peripheral circulation either from a
subcutaneous depot or as an intravenous slow infusion. The result is that
only about 10 percent of the administered dose of insulin reaches the
liver as compared to approximately 50 percent in normal persons. As a
consequence, hepatic glucose production is not first reduced; rather,
blood glucose is lowered by increased utilization by other tissues
(muscle, fat) as a result of the presence of high levels of insulin in the
peripheral circulation. Accordingly, normal levels of blood sugar are
achieved only by carefully matching any increased peripheral utilization
of blood sugar to an increased hepatic production, which is inherently
much more difficult than simply decreasing hepatic glucose production.
When demand for blood sugar exceeds the supply (as a result of too much
insulin injected), the blood glucose drops below normal values. There is
little glucose reserve since the liver, in its state of
under-insulinization, is already releasing glucose. The result is that the
blood sugar level will plummet despite adequate levels of
counterregulatory hormones (glucagon, epinephine, norepinephine, and
growth hormone) whose actions are to increase liver production of glucose
in emergency situations. This hypoglycemic reaction, a progression of
symptoms from nervousness, sweating, stupor, unconsciousness, and
occasionally, irreparable brain damage, will occur until sugary substances
are taken by mouth or intravenously.
The ongoing cycle between hyperglycemia and hypoglycemia has created a
basic rift in the philosophy of diabetic control. The "tight control"
philosophy claims that the long-term devastations of diabetes (blindness,
heart attacks, kidney failure, and loss of extremities) are due to
abnormally elevated sugar levels, and strives to keep blood sugar within
the normal range even at the risk of frequent (more than once a week)
hypoglycemic reactions. The converse of the foregoing is the "loose
control" philosophy which is based on the presumption that the basic
foundation of the tight control philosophy has yet to be proved and that
the considerable risks of hypoglycemic reactions are not worth an unproved
benefit.
The intraperitoneal delivery of insulin has recently been investigated as
an alternative to both the intravenous and subcutaneous delivery sites.
Although access to the intraperitoneal site is more difficult, it has the
potential advantages of avoiding peripheral hyperinsulinaemia (high blood
insulin levels), insulinizing the liver via direct portal venous system
insulin absorption, and more rapid absorption than subcutaneously
delivered insulin. Preliminary results appear favorable for
intraperitoneal delivery of insulin.
Insulin delivery into the peritoneum is reported to have resulted in a
rapid rise in circulating peripheral insulin concentration, which peaked
at 30-45 minutes following the initiation of insulin delivery.
Furthermore, when the infusion rate of intraperitoneal insulin was reduced
to the background rate, a gradual decline in peripheral insulin
concentration to normal fasting values resulted. (This free insulin
response contrasted to the continuing high levels following subcutaneous
insulin injection.) It was, therefore, concluded that normalization of
plasma insulin profiles was achievable with intraperitoneal infusion of
insulin and, further, that meal-related hyperglycemia (elevated blood
glucose) is well-controlled with intraperitoneal insulin and yet
hypoglycemic episodes are reduced compared to subcutaneous delivery. For
reference, see "Normalization of Plasma Insulin Profiles With
Intraperitoneal Insulin Infusion in Diabetic Man," D. S. Schade, R. P.
Eaton, N. M. Friedman, and W. J. Spencer, DIABETOLOGIA, 19, 35-39 (1980).
The peritoneum is the largest serous membrane in the body and consists, in
the male, of a closed sac, a part of which is applied against the
abdominal parietes, while the remainder is reflected over the contained
viscera. In the female, the peritoneum is not a closed sac, since the free
ends of the uterine tubes open directly into the peritoneal cavity. The
part which lines the abdominal wall is named the parietal peritoneum and
that which is reflected over the contained viscera constitutes the
visceral peritoneum. The space between the parietal and visceral layers of
the peritoneum is named the peritoneal cavity. However, under normal
conditions, this cavity is merely a potential one, since the parietal and
visceral layers are in contact.
For a number of years, it has been well-known that the peritoneal membrane
will function fairly effectively as an exchange membrane for various
substances. As early as 1923, peritoneal dialysis (an artificial kidney
format) was first applied clinically. The first peritoneal access device
was a piece of rubber tubing temporarily sutured in place. In 1960,
peritoneal dialysis was becoming an established form of artificial kidney
therapy and, in order to lessen the discomfort of repeated, temporary
punctures into the peritoneal cavity, various access devices permitting
the painless insertion of the acute or temporary peritoneal catheters were
developed.
The most common peritoneal access device is of the Tenckhoff type: a capped
percutaneous (through the skin) silastic tube passes through the abdominal
wall into the peritoneal cavity.
Another peritoneal access device (the "Gottloib" prosthesis) consists of a
short, "golf tee" design that is adapted to be placed under the skin with
a hollow tubular portion extending just into the peritoneal cavity. This
device is designed specifically to allow the insertion of an acute
peritoneal catheter (a Trocath) through the skin and down through this
access tubing directly into the peritoneal cavity. Another device consists
of a catheter buried underneath the skin and extending into the peritoneal
cavity via a long tubing. Peritoneal dialysis is performed by inserting a
large needle into the subcutaneous portion of the catheter.
All of the devices known were designed with one purpose in view: peritoneal
dialysis, and are used almost exclusively by one group of patients, those
with End-Stage Renal Disease (ESRD), whose kidney function will never
return. In simple terms, therefore, the access devices to the peritoneal
cavity plus the peritoneal cavity itself constitute an artificial kidney.
A variety of drugs or other fluids are frequently added to the large
volumes of peritoneal dialysis solutions and are thus instilled (injected)
into the peritoneal cavity for various therapeutic reasons. Some examples
of these drugs are antibiotics, amino acids, and insulin (for diabetics).
However, such therapeutic maneuvers are fortuitous in that the clinician
is simply taking advantage of a particular situation, that is, a
peritoneal access device emplaced in a particular group of patients.
In spite of the foregoing, there are cogent reasons for not using existing,
permanent peritoneal accesss devices for simple drug injections in a wide
variety of patients not suffering ESRD. Most of these devices have what
might be termed a relatively large internal volume, that is, it would
require anywhere between about five and twenty milliliters, (depending
upon the device), to fill the device with fluid. This volume which is a
dead volume or dead space, is a very real hindrance in that the injected
fluid may simply remain within the device itself instead of entering the
peritoneal cavity.
In view of the foregoing, it would be an advancement in the art to provide
a novel subcutaneous peritoneal injection catheter which may be readily
implanted underneath the skin and provide direct access into the
peritoneal cavity. It would also be an advancement in the art to provide a
subcutaneous peritoneal injection catheter having a relatively small
internal volume while providing a relatively enlarged target area. Such a
novel subcutaneous peritoneal injection catheter apparatus and method is
disclosed and claimed herein.
BRIEF SUMMARY AND OBJECTS OF THE INVENTION
The present invention relates to a novel subcutaneous peritoneal injection
catheter apparatus and method, the apparatus including a receiving chamber
or reservoir having a relatively small internal volume while employing a
penetrable membrane as relatively enlarged target surface area. The
reservoir is interconnected with the peritoneal cavity by a hollow stem.
The penetrable membrane accomodates a hollow needle being inserted into
the receiving reservoir and is configurated with a dome-like profile so
that the membrane may also be depressed to expel insulin from the
receiving reservoir into the peritoneal cavity. Portions of the catheter
are covered with a velour surface to accomodate tissue ingrowth and
securement of the catheter subcutaneously.
It is, therefore, a primary object of this invention to provide
improvements in implantable injection catheters.
Another object of this invention is to provide an improved method for
injecting fluids into the peritoneal cavity.
Another object of this invention is to provide a novel subcutaneous
peritoneal injection catheter having a relatively small fluid capacity
while presenting a relatively large target surface area.
Another object of this invention is to provide a novel peritoneal catheter
having a receiving reservoir and a dome-like cover for the receiving
reservoir, the dome-like cover serving as an expulsion membrane for
forcing fluids from the receiving reservoir into the peritoneal cavity.
Another object of this invention is to provide an implantable injection
catheter having securement means for securing the catheter subcutaneously.
These and other objects and features of the present invention will become
more fully apparent from the following description and appended claims
taken in conjunction with the accompanying drawing.
BRIEF DESCRIPTION OF THE DRAWING
FIG. 1 is an exploded, perspective view of the stem, body and cover that
provide the basic structure of the novel peritoneal catheter of this
invention;
FIG. 2 is a cross-sectional view taken along lines 2--2 of FIG. 1;
FIG. 3 is a perspective view of the novel peritoneal catheter of this
invention with portions broken away to reveal internal construction;
FIG. 4 is a schematic illustration of the novel peritoneal catheter of this
invention shown implanted in the abdominal wall of a torso;
FIG. 5 is a cross-sectional, schematic illustration of the novel peritoneal
catheter of this invention implanted in the abdominal wall and shown in
cooperation with a hypodermic syringe; and
FIG. 6 is a cross-sectional, schematic illustration of the novel peritoneal
catheter of this invention implanted in the abdominal wall and being
compressed to expel fluids therefrom into the peritoneal cavity.
DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS
The invention is best understood by reference to the drawing wherein like
parts are designated with like numerals throughout.
GENERAL DISCUSSION
As a general restatement, diabetes is generally identified as a metabolic
disorder in which the ability to metabolize carbohydrates and, more
particularly, glucose, is more or less completely lost due to faulty
pancreatic activity and consequent disturbance of normal insulin
mechanism. Insulin acts by regulating the metabolism of glucose, and there
is evidence that it does this by facilitating the transport of glucose
through the cell membrane. A corollary hormone, glucagon, acts by
stimulating the conversion of glycogen into glucose by activating liver
phosphorylase. The subsequent release of glucose into the bloodstream
causes a hyperglycemic effect which is thus opposite to the hypoglycemic,
or blood-sugar-lowering effect, of insulin. It appears that there is a
natural balance of action of the two hormones resulting in the control of
glucose release and utilization. Insulin is secreted by certain cells of a
pancreatic tissue known as the Islets of Langerhans. A deficiency of these
cells and consequent decrease in insulin secretion has been found in human
subjects who developed diabetes at a relatively young age. Such patients
usually suffer an almost total lack of insulin and are designated as
"juvenile onset diabetics" or "ketosis-prone diabetics." Such patients die
if not treated by insulin injections.
Routine administration of insulin used to treat patients with ketosis-prone
diabetics leaves much to be desired. Once or twice daily injections with
any of the long-acting insulins, although continuous in a basal sense,
makes no pretense at supplying controlled variable amounts of insulin
consequent upon changing metabolic demands. Furtheremore, aggressive
peripheral insulin administration (that is, insulin injected
subcutaneously, intramuscularly or intravenously), used in an attempt to
obtain tight control of glycemia, may lead to periods of sustained
hyperglycemia that occasionally cycles into a hypoglycemic state. It is
possible that changes in circulating, metabolically active hormones and/or
receptor site concentrations are responsible for this situation.
Possibly the major problem encountered in controlling glycemia is the
unphysiological administrative route of therapeutic insulin. The liver,
the prime organ involved in regulation of blood glucose levels, is
initially bypassed following injection by the peripheral route
(subcutaneous, intramuscular, intravenous). Achieving normoglycemia by
injection of peripheral insulin inevitably engenders high blood insulin
levels (hyperinsulinemia). The physiological insult imposed by
hyperinsulinemia perturbs many metabolic feedback loop controls, which in
turn lowers the gain of this web of servo mechanisms. The end result is
that good, sustained control of glycemia is achieved at the expense of a
razor-thin margin between normoglycemia and hypoglycemia. Prolonged
hypoglycemia kills people, so diabetologists over the years have generally
followed safety-first rules: allow the patient to function in a controlled
hyperglycemic state. However, the evidence is now tilting towards a
prolonged, if controlled, hyperglycemic state as being at least part of a
general metabolic derangement, which causes longterm accelerated vascular
and peripheral nerve pathology.
In an effort to regulate these undesirable alternatives
(hyperglycemia.revreaction.hypoglycemia), various closed and open loop
control delivery systems have been developed. Yet the therapists involved
still persist in using these systems to deliver insulin peripherally.
Closed loop delivery systems are synonymous with prolonged
hospitalization: open loop delivery systems actually produce a more
sustained, if somewhat better regulated, hyperinsulinemic state.
Additionally, they are awkward to wear, they require tubing sets and
implanted needles and, in spite of claims made to the contrary, they can
malfunction ("surge"), usually at the most inconvenient hours.
Portal venous administration of insulin has given highly encouraging
results in experimental animals: less insulin is required to achieve
normoglycemia and hyperinsulinemia is avoided. However, long-term access
directly into the portal system carries several severe risks all of which
are lethal. Nevertheless, there is a secondary and much safer route
leading directly into the portal system: the visceral (that covering most
of the gut) peritoneal membrane.
Intraperitoneal Insulin. Intraperitoneal delivery of insulin has been
performed in ketosis-prone diabetic human subjects on a short-term (hours)
basis, achieving comparable glycemic control to that achieved with
subcutaneous insulin, yet with only approximately half the integrated
blood levels of plasma insulin. Intraperitoneal insulin has also been
utilized long term in patients with ketosisprone diabetes and end-stage
renal disease treated by continuous ambulatory peritoneal dialysis. (An
artificial kidney format). Adequate control was achieved in the three
patients reported.
There is no readily available documentation substantiating the thesis that
the intraperitoneal delivery of drugs is primarily absorbed into the
portal venous system (visceral peritoneum) rather than the general
systemic venous system (parietal peritoneum). However, there is a
considerable amount of indirect evidence for this hypothesis: (1) at
laparotomy one's field of vision is virtually totally obscured by
mesenteric (visceral) peritoneum; (2) the work of other researchers
indicates that control of glycemia by intraperitoneal insulin is good yet
there was a 50% "loss"--presumably picked up by the liver before reaching
the peripheral circulation; (3) intraperitoneal administration of sodium
nitroprusside (for the purpose of causing intraperitoneal vasodilatation)
resulted in no detectable levels of peripheral plasma thiocyanate: it is
assumed that metabolism of nitroprusside by the liver accounted for the
lack of peripheral thiocyanate. One researcher stated that he had always
presumed intraperitoneal administration of drugs resulted in their direct
transfer to the portal venous system but had never tested the hypothesis
directly nor could he think of anyone else who had done so.
One final point must be made: Intraperitoneal administration of various
dialysis fluids and certain drugs such as antibiotics, permanent access to
the peritoneal cavity and knowledge of the physiological migratory route
of insulin have been with us for many years. Therefore, why has not
intraperitoneal delivery of insulin been utilized in the past? In fact,
this route has been used in patients who are diabetic and suffering
end-stage renal disease (ESRD). However, until recently, chronic
peritoneal dialysis was performed on an intermittent basis (once, twice or
thrice weekly), which encouraged only widely spaced use of intraperitoneal
insulin. Also, peritoneal dialysate was supplied in glass bottles and
insulin sticks to glass in quite substantial amounts. Finally, until
recently there were very few diabetic patients treated for ESRD.
The major impediment to utilizing the intraperitoneal route for delivery of
insulin in patients not suffering ESRD is lack of a suitable
intraperitoneal access device. The majority of standard peritoneal
catheters are long, clumsy, percutaneous, infection-prone silastic tubes.
One balks at the thought of any patient wearing one of these unless
absolutely necessary.
The present invention is a peritoneal access device with the following
constraints. (1) The dead space or dead volume of the device is minimal.
(2) It presents a large surface area (consistent with the first
constraint) to allow for injection of various drugs. (3) It is designed
purely and simply for one-way flow, i.e., drug injection is inward only;
there is no outflow considered. (4) It is designed so that a variety of
drugs may be injected into the peritoneal cavity. (5) It has a resilient,
dome surface above the receiving reservoir so that the dome may be
depressed to expel insulin from the receiving reservoir into the
peritoneal cavity. (6) It is not designed for peritoneal dialysis and, in
fact, would not function if used for this purpose.
The Preferred Embodiment
Referring now more particularly to FIGS. 1 and 2, the peritoneal catheter
apparatus of this invention is shown generally at 10 and includes a stem
12, a body 14, and a cap 16. Stem 12 is configurated as a hollow, tubular
column 42 having a diametrally enlarged base 44 at one end and a hollow
lumen 40 extending therethrough. Column 42 is shown broken in FIGS. 1 and
2 to demonstrate that its length is adjustable. Importantly, it is
possible to selectively predetermine the length of column 42 and thereby
adapt peritoneal catheter 10 for implantation in an abdominal wall 22
(FIGS. 4-6) having any suitable thickness as will be discussed more fully
hereinafter. Base 44 is formed as a diametrally enlarged flange that
serves as a retention member to inhibit peritoneal stem 12 from being
completely withdrawn into the tissue of abdominal wall 22 with a
corresponding loss of fluid communication through lumen 40 into peritoneal
cavity 34 (FIGS. 4-6).
Body 14 serves as the basal member for peritoneal catheter 10 and is
configurated with a funnel-like section 52 having a relatively shallow
depth in comparison with the relatively enlarged diameter. The depth of
funnel section 52 is selectively predetermined so as to contain a
predetermined body of insulin which may b | | |
