Case 186: An Ulcerated-Abscessed-Ischemic-Neuropathic Foot Finally Healed after Release of Achilles Tendon.

At age 65, this lady was admitted to the Bryn Mawr Hospital on an urgent basis on December 30th, 1993 because of an abscessed swollen foot. She stood 59.2 inches (150 cm) tall and weighed about 105 Lb. (47.7 Kg) at age 18. She weighed perhaps 125 Lb. (56.8 Kg) at age 25 when she was married. Over the years she increased her weight to 200-210 lb. (91-95.5Kg) and about age 40 developed diabetes. The latter was treated by her family doctor with oral agents and in the last ten years prior to this admission with "perhaps" insulin. Around the time of Christmas 1992, she had developed a sore on the plantar surface of her foot that brought her into the hospital under the care of her family doctor and a consulting plastic surgeon.

February 8th, 1993: Charcot changes in the midfoot were seen. Bone fragments, soft tissue swelling and the outline of her plantar ulcer were seen in the midarch.

After a course of antibiotics, the plastic surgeon grafted skin from her thigh to the bottom of her foot where it initially did well. However, with ambulation the graft broke down and she again continued with her life having a chronic plantar ulceration. Around Christmas 1993, she noted her toes were getting red and she lost her appetite. She consulted her physicians by phone and was advised to lower her insulin. Finally, on December 30th, she consulted her plastic surgeon who noted her badly abscessed foot and personally delivered her to our Bryn Mawr office on the evening of December 30th.

Her medications included both NPH and regular insulin (34 N and 16 R in the morning and 16 N and 4 R before supper), vitamins, and Aldactone (spironolactone) 25 mg three times a day. She was an active smoker and drank modest amounts of coffee. She had consulted a dermatologist for leg pigmentation and been advised she had diabetic dermopathy. She had had cataracts removed and claimed to have good vision.

General Physical findings: She was febrile, obese and pale. She had no obvious retinopathy. Her breath sounds were diminished and she had diffuse fine rales. Faint bruits were present in both carotids. She had a basal systolic ejection sound perhaps related to her hyperdynamic state. Her abdominal panniculus extended over her flanks and over her pubic area. Her femoral pulses were 2+ while distal pulses were absent. Sensation in her feet was absent; she could not feel either a stick or cotton.

December 30th, 1993: Presenting with an ulcerated abscessed foot.

December 31th, 1993: The soft tissue swelling is well appreciated in her foot x-ray.

Films of her good foot are shown for comparison.

Notice how the bones are well delineated. The calcaneous has a slight upper tilt. The arch is well preserved. Her hammer toes point upward in respect to her metatarsals.

Right Foot Lesions and Initial Treatments: She had a large ulcer on the plantar surface of the proximal third of her right foot. The right foot was misshapen and swollen. At the base of the first toe she was draining pus. Copious amounts of pus was elicited by pressing under the first metatarsal head and over the dorsum of the foot; the pus was cultured. A small incision was made over the first metatarsal head releasing more pus; the incision was irrigated with Sea Soaks containing gentamicin until the return was clear. A fluctuant area the size of a golf ball on the dorsum of the foot was aspirated with an 18-gauge needle, again recovering about two ounces (60 ml) of ketchup-like pus. This area was also irrigated until clear. She was then given 1500 mg of Augmentin orally. Her foot was reduced in size somewhat but still remained relatively swollen. A vial of gentamicin (80 mg) was injected into multiple sites in the two abscessed areas and 40 mg was injected into 3-4 sites in the plantar ulcer. The rim of callus around the ulcer was debrided until the skin was smooth and soft. The foot was then immersed in a cleansing bath of Sea Soaks and dilute peroxide. Then, her foot was placed in a clear plastic bag containing Sea Soaks and gentamicin and the bagged foot was placed in the Mini-Boot and pumped for 40 minutes to disseminate the injected antibiotic around the tissue planes of her foot, further reduce swelling, and maintain the arterial flow in the foot. She tolerated the procedures well, but because of the gravity of her situation, she was transferred from the office to the hospital for further treatments.

Hospital Course Her initial laboratory studies were cause for alarm: Her leukocyte count was 16.6 with a strong shift to the left: 93% polys, 4% bands, 2% lymphs and 1% monos. Her prothrombin time was prolonged in the absence of anticoagulant therapy. Her serum electrolytes were abnormal (sodium 129 mEq, BUN 51 mg/dl and creatinine 2.1 mg/dl). Her albumen was low (1.9 G/dl) and both bilirubin (2.3 mg/dl) and alkaline phosphatase (196- 304) high. Her urinary urobilinogen was increased to 4 mg (normal < 2mg/dl). Once in her hospital gown, it was apparent she had metastatic infections: the dorsum of her left hand was ruborous and puffy with apparent cellulitis extending from the bases of the 3rd and 4th fingers to her wrist and the dorsum of her left foot was red and exuding pus. Eventually the several cultures from both feet returned showing abundant Beta Streptococcus, group G. Her systemic antibiotic coverage was Timentin 3.1 grams every 8 hours intravenously. The abscess cavities in her right foot were irrigated every 8 hours by the nursing staff. The booting staff also injected her foot with gentamicin and pumped it in the Mini-Boot in a bath of Sea Soaks containing gentamicin and Urecholine. The left hand was thought to have good arterial circulation and was given hot soaks. The left foot continued to worsen in spite of the intravenous antibiotics; after the 4th hospital day, hence, it too was treated with local antibiotics and Mini-Boot therapy and immediately improved. Perhaps related to her coagulopathy and a few uterine fibroids seen on ultrasound, her early course was also accompanied by modest vaginal bleeding.

Insurance Woes: On the 3rd hospital day a physician from her insurance company ("company doc") called her attending physician ("patient doc") and instructed him to discharge the patient. The patient doc refused claiming the patient was too sick to go home. The company doc said the insurance company would no longer cover the hospitalization. The patient doc said he would then call the local newspapers and report how the insurance company was throwing this sick women into the streets. The company doc said the patient doc did not want to do that. He would do that, the patient doc insisted. After further discussion, they agreed that the company nurse, who reviewed the patient chart in the hospital to keep the company docs abreast of the status of the patient, would call the patient doc when she was next in the nursing station. And, the next day in the midst of the patient doc's office hours she did indeed call. The patient doc went to the hospital and educated the nurse: the temperature chart showed spiking fever; the infection was still not controlled; her metastatic infections and coagulopathy raised the possibility of a septic death; her diabetes required close regulation that the patient was too sick to attend; with her low albumen , she was leaking fluid into various tissue spaces and was being given albumen intravenously to correct the problem; the systemic antibiotics were not successfully reversing her infection and the patient was too sick to travel to the office for daily boot treatment. The company nurse actually paled when she understood the import of the data on the chart. The next day the company doc again called the patient doc and allowed that the patient could stay another three days. The patient doc said it was very unlikely that a lady this sick would be ready for discharge in less than three weeks. And the company doc telephoned yet a third time. This time he advised the patient doc that the insurance company was preparing a list of preferred doctors for their subscribers and that the cooperation of the patient doc was being observed. Thank you for the information, said the patient doc... who it appears remains off the list still today. The patient changed insurance companies.

January 10th, 1994: Her foot swelling was reduced. Her bony structures were better delineated. But her calcaneous did not have the normal upward tilt seen in the good foot. A bony fragment was present in the arch in line with the tibia. The soft tissue swelling in the arch gave her a rocker foot. One could appreciate that her plantar ulcer might not heal with ambulation.

November 11, 1994. Callus had formed and broken down under the bony prominence in her midfoot.

March 13th, 1995. Persistent ulceration and callus.

November 1996. Histologicly, the material debrided from the arch area looked like a wart to the pathologist. The rest of the skin of the foot was healthy.

October 1997. The callus was regularly trimmed back and the wart area debrided back to healthy tissue. Still with regular ambulation, the ulcer persisted and enlarged.

February 1999. The orthopod cut her Achilles tendon. Her calcaneous assumed a more normal position and the ulcer is here shown close to being healed.

Our orthopedic consultant finally recommended that we release her Achilles tendon to allow her posterior heel to drop and the distal plantar aspect of the calcaneous to rise hopefully ridding her of the pressure point in her midfoot. During this interval, her other medical problems also required attention. She was hospitalized in November 1995 with pleural effusions, thrombocytopenia, chronic obstructive pulmonary disease (49 pack years of smoking). With the addition of diuretics to her program her BUN rose from 19 to 30 and her creatinine from 1.3 to 1.9 mg/dl during the hospitalization. On October 3rd, 1997 her BUN, creatinine and PO4 were found to have risen to 110, 3.1 and 6.5 mg/dl respectively. Her diuretics were decreased. She was given a diet low in protein and phosphorus. She was encouraged to maintain hydration adequate to make at least 1.5 L/day and she was given long boot treatments. Her renal function studies improved and her BUN and creatinine have been maintained in the range of 46 to 55 and 2.0 to 2.5 from March 1998 to present.

Comments: This lady is presented to illustrate many points. First, local antibiotics and booting played a crucial role in curing her initial infection and saving both legs... if not her life. Second, her problem with the insurance company was not just due to greed and arrogance on the part of the insurance company; the nurses advising the company doctors are commonly not sufficiently skilled to properly evaluate the patient and the insurance company doctor may also not be skilled in the issues he/she are asked to judge. This is a case of "managed care" going awry. Next, this is another patient whose heart and kidney function benefited from her boot therapy. Finally, she aptly demonstrates that booting is not everything. Orthopedic problems (in this case a bony prominence) may have to be addressed also. With booting this lady has had the use of her legs for over five years. Hopefully now she will be free of ulcers.